Gastrointestinal

Question 1

organs of GI sys

Answer 1

digestive organs:
* oesophagus
* stomach
* small intestine (SI)
* large intestine (LI)

accessory organs:
* pancreas
* liver

Question 2

physiology of how digestion occurs

Answer 2

1. motility - how food moves thru
2. digestion
   * digestion = chem breakdown by enzs
   * absorption (once small enough units) - selective
   * metabolism - what used for once in bloodstream
   * egestion (defaecation)

Question 3

stages digestion

Answer 3

1. mechanical breakdown - prehension (food into mouth), mastication, motility
2. chem breakdown - secretion, digestion

Question 4

how do animals do prehension

Answer 4

tongue, lips, head movement

Question 5

rough outline motility

Answer 5

move food gradually thru GI tract, absorb what want (once small enough), leave waste

Question 6

which digestive process at each location

Answer 6

1. teeth (mechanical)
2. salivary glands - secretion
3. stomach (motility, secretion)
4. liver/gall bladder/pancreas - secretion
5. SI - motility, digestion, absorption
6. LI - motility, fermentation, absorption, egestion

Question 7

what is secreted in saliva

Answer 7

mostly environ for enzs work - some species enzs asw (e.g. amylase) but often not there long enough
* plus mucous to lubricate food

Question 8

egestion vs excretion

Answer 8

both getting rid waste substances
* egestion = allowing waste pass out
* excretion = removal once absorbed bloodstream

Question 9

saliva types + where proded

Answer 9

• parotid = serous
• mandibular/buccal/sublingual = mucous + serous
• simple-stomached = mostly mucous, pH neutral
• complex-stomached = mainly serous for optimum fermentation, pH alkaline

Question 10

serous vs mucous saliva

Answer 10

serous = more liquidy, balancing pH (ruminants more)
mucous for lubrication + conts amylase so for diets low starch (not ruminants)

Question 11

why are digestive secretions reabsorbed

Answer 11

prevent dehydration
* not reabsorbed = diarrhoea

Question 12

composition saliva

Answer 12

• 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

Question 13

saliva secretion non-ruminants in reference to blood

Answer 13

• primary secretion isotonic blood
• low flow (not eating) = hypotonic bc minerals reabsorbed blood
• high flow = remains isotonic bc no time + reabsorbs later

Question 14

saliva secretion ruminants

Answer 14

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

Question 15

how is salivary secretion regulated

Answer 15

under neural control ANS
* sympathetic = fight/flight = prod reduced
* parasymp = rest/digest = prod inc

Question 16

reflex pathways salivary secretion types

Answer 16

1. congenital = innate, from taste, afferent to salivary centre brain, efferent to salivary glands
2. conditioned = learned, Pavlov, initiated cerebral cortex, then salivary centre in medulla oblongata

Question 17

types motility movements digestion

Answer 17

• segmental contractions = mech breakdown
• peristaltic contractions
• anti-peristaltic contractions
• mass movement

Question 18

peristaltic contractions =?

Answer 18

movement general aboral direction (away from mouth) at rate allow sufficient time digestion + absorption

Question 19

how do segmental contractions work

Answer 19

mech breakdown at one place

Question 20

anti-peristaltic contractions

Answer 20

movement food oral direction bc:
* slow transit digesta for sufficient digestion + absorption - longer in GI tract
* allow rumination
* protective - e.g. vomiting

Question 21

what is mass movement

Answer 21

extended peristaltic contraction to empty sections GI tract + give space new food - e.g. colon for defaecation
* still aboral direction

Question 22

how is motility regulated

Answer 22

chewing, swallowing, defaeaction (not horses) under voluntary control
intestinal contractions involuntary control (sm musc)

Question 23

what causes chem breakdown

Answer 23

• secretion digestive juices
• salivary/liver/pancreas/stomach + intestinal wall glands

Question 24

purpose mucus in digestive juices

Answer 24

1. lubricate food
2. protect mucosa from ulcerations - particularly stomach

Question 25

important carb digestive enzs + where?

Answer 25

amylase + disaccharidases (to monosacchs) * saliva * pancreas * intestinal mucosal surface

Question 26

prot digestive enzs + where?

Answer 26

pepsin, trypsin, peptidases (-> small enough absorb) * stomach glands * pancreas * intestinal mucosal surface

Question 27

fat digestive enzs + where

Answer 27

lipase, phospholipase * pancreas * intestinal mucosal surface

Question 28

how are nutrients absorbed

Answer 28

* mostly active transport against conc grad - mostly secondary, some primary * passive transport facilitatively via transporter prot, or diff

Question 29

layers abdominal wall

Answer 29

* skin - hair for insulation as traps air (dense = fur, wool = type) * subcutaneous fascia * muscles

Question 30

layers subcutaneous fascia

Answer 30

* 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

Question 31

4 muscles abdominal wall

Answer 31

LATERAL (outside to inside) 1. external abdominal oblique 2. internal abdominal oblique 3. transverse abdominal VENTRAL: rectus abdominis

Question 32

functions abdominal wall

Answer 32

* 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

Question 33

rectus abdominis

Answer 33

straight, originating sternum * inserting on cranial border pubis via pre-pubic tendon * L + R sepped linea alba (line middle 6 pack) | 6 pack

Question 34

external oblique abdominal musc

Answer 34

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)

Question 35

internal oblique abdominal musc

Answer 35

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)

Question 36

transverse abdominal musc

Answer 36

innermost lateral abdominal wall musc * originates on medial surfaces ventral parts caudal ribs + deep lumbodorsal fascia * inserts on linea alba * fibres run dorsal -> ventral

Question 37

sheath rectus abdominis musc

Answer 37

formed from tendons lateral abdominal wall muscles, passing above/below rectus abdominis musc to join in midline

Question 38

where sheath rectus abdominis joins midline+ how

Answer 38

aponeurosis + forms linea alba

Question 39

how sheath rectus abdominis varies

Answer 39

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

Question 40

how are abdominal wall muscles innervated

Answer 40

spinal nerves last thoracic vertebra + L1-L5 1. dorsal roots innervate dorsal musculature 2. ventral roots split 3 branches

Question 41

3 branches vetral root innervation abdominal wall musc

Answer 41

1. medial bet TA + IAO down to RA 2. lateral bet IAO + EAO down to midway 3. lateral cutaneous perforates EAO to innervate skin

Question 42

what forms gut (embryologically)

Answer 42

endoderm = epithelium lining GI tract + associated exocrine glands mesoderm = musc + CT embryo develops + part yolk sac taken into bod - forms gut

Question 43

how does yolk sac in bod form gut

Answer 43

* midgut sepped foregut/hindgut by cranial/caudal intestinal portals * forgut/hindgut end blindly at oral/cloacal plates - will later perforate

Question 44

which organs does foregut diff into

Answer 44

* pharynx * oesophagus * stomach * initial duodenum

Question 45

what does midgut diff into

Answer 45

* rest duodenum * jejunum * ileum * caecum * ascending/transverse colon

Question 46

what does hindgut diff into

Answer 46

* descending colon * rectum

Question 47

how does foregut develop

Answer 47

* stomach rotates sideways + backwards + enlarges as storage organ * pancreas develops - initially 2 sep organs, hence 2 secretory pts

Question 48

blood supply to foregut

Answer 48

branches from celiac artery

Question 49

development midgut

Answer 49

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

Question 50

result midgut rotation

Answer 50

* colon quite cranial + caecum RHS * twisted round central pt where CMA branches off aorta

Question 51

blood supply to midgut

Answer 51

branches cranial mesenteric artery

Question 52

general development hindgut

Answer 52

1. bud from ventral part = allantoid (precursor umbilical cord) 2. urorectal septum enlarges + divides 2 sep tubes 3. = when born faecal + urinal waste can be sepped

Question 53

blood supply to hindgut

Answer 53

branches caudal mesenteric artery

Question 54

topographical anatomy

Answer 54

where something located in relation to space its in

Question 55

peritoneum

Answer 55

single serous mem that lines abdominal cavity + envelops abdominal organs * parietal closely adheres abdominal wall * visceral closely adheres organ surface * connecting bet the 2

Question 56

connecting peritoneum types

Answer 56

1. mesentery connects bowel (SI + LI) to body wall 2. omentum connects stomach to something 3. fold connects bowel to bowel 4. ligament connects non-bowel to something

Question 57

what defines abdominal cavity

Answer 57

peritoneal attachments - some organs tightly held in position, others loosely

Question 58

what defines abdominal cavity

Answer 58

* diaphragm cranially * abdominal wall laterally * conts all organs inc peritoneum

Question 59

define peritoneal cavity

Answer 59

* conts nothing, potential space bet parietal + visceral peritoneum * small amount peritoneal fluid - lots = inflammation = peritonitis

Question 60

structure + location diaphragm

Answer 60

* seps thorax + abdomen, attaching body wall at level last rib * extends into thorax to level 5th intercostal rib * musc outside, central tendon

Question 61

holes in diaphragm

Answer 61

1. aorta passes thru aortic hiatus bet L + R crura 2. caudal vena cava thru caval foramen in central tendon 3. oesophagus thru oesophagal hiatus

Question 62

structure liver

Answer 62

4 lobes: * L + R lobes - split medial + lateral sometimes * caudate - split caudate + papillary processes * quadrate

Question 63

when do L + R lobes of liver split

Answer 63

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

Question 64

gall bladder role + parts

Answer 64

stores + concentrates (no synth) bile has cystic, hepatic + common bile ducts

Question 65

peritoneal attachments liver

Answer 65

1. coronary ligament - circular around vena cava 2. R + L trinagular ligaments = tight attachments to diaphragm 3. falciform/round ligament to ventral body wall at umbilicus * loose but liver so firmly attached elsewhere no matter | firmly attached diaphragm = hard access surgery

Question 66

what does round ligament mean

Answer 66

foetal remnant - round ligament liver was umbilical vein

Question 67

location + parts adult stomach

Answer 67

runs L -> R across abdomen 1. fundus = blind ending 2. corpus 3. pylorus (pyloric antrum)

Question 68

peritoneal attachments stomach

Answer 68

1. greater omentum = greater curvature stomach -> dorsal body wall 2. lesser omentum = lesser curvature stomach -> liver (= hepato-gastric ligament) 3. gastro-splenic ligament -> spleen

Question 69

regions embryo that give rise stomach + epithelium types cause

Answer 69

1. oesophageal -> stratified squamous 2. cardiac -> glandular (mucous) 3. fundic -> glandular (mucous/HCl/pepsinogen) 4. pyloric -> glandular (mucous)

Question 70

what areas of adult stomach derived from which embryological areas | table

Answer 70

Question 71

omental bursa

Answer 71

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

Question 72

where is spleen located + attached + purpose

Answer 72

LHS abdomen * peritoneal attachment = gastro-splenic ligament * blood reservoir * v mobile + can get in way

Question 73

duodenum is + what joins?

Answer 73

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

Question 74

peritoneal attachments duodenum

Answer 74

* mesoduodenum -> body wall * duodeno-colic fold -> colon * hepato-duodenal ligament (part lesser omentum) -> liver

Question 75

pancreas structure

Answer 75

2 lobes: * R running cranio-caudal * L running medio-laterally

Question 76

peritoneal attachments pancreas

Answer 76

* R lobe w/in mesoduodenum * L lobe w/in deep fold (leaf) greater omentum

Question 77

what is jejenum

Answer 77

middle part SI (80% of it), covered greater omentum

Question 78

peritoneal attachment jejenum

Answer 78

meso-jejunum = mesentery * attaches at single pt dorsal abdom wall + fans out along length

Question 79

ileum

Answer 79

last part SI, enters LI at caeco-colic junction

Question 80

peritoneal attachments ileum

Answer 80

* ileo-caecal fold - attached caecum * meso-ileum (extension meso-jejunum)

Question 81

caecum

Answer 81

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

Question 82

peritoneal attachments caecum

Answer 82

* ileo-caecal fold * caeco-colic fold

Question 83

colon structure

Answer 83

* ascending (right) = up right side * transverse along * descending (left) = down left side -> rectum R + L colic flexures on either side where changes direction

Question 84

# [](http://) peritoneal attachments colon

Answer 84

meso-colon = to dorsal body wall

Question 85

what do sensory cells GI tract detect

Answer 85

* wall stretch * nutrient conc * metabolite conc * osmolarity * pH * irritation of mucous mem | no pain receptors w/in abdomen

Question 86

how are reflexes GI tract initiated

Answer 86

* stimulation sensory cells * CNS at sight/smell food + in regulation appetite

Question 87

how are digestive processes coordinated

Answer 87

neural + hormonal regulation | negative feedback mechanisms

Question 88

enteric nervous sys (ENS)

Answer 88

GI tract's own NS, entirely w/in its wall = guts keep working independently w sensory + motor neurones in its wall = **short reflex arcs**

Question 89

what do sensory cells ENS respond to

Answer 89

1. content lumen 2. degree wall stretch

Question 90

what do motor cells ENS stim

Answer 90

1. smooth musc cells for motility 2. epithelial cells to secrete digestive juices (-> lumen gut) + hormones (-> blood)

Question 91

nerve plexus

Answer 91

intersecting bundle nerves

Question 92

long reflex arcs of GI sys

Answer 92

part ANS, connect in CNS * symp halts digestion * parasymp promotes digestion (rest/digest)

Question 93

reflex arcs illustrated | diagram

Answer 93

Question 94

why short reflex arcs good

Answer 94

give GI tract extensive control of activities

Question 95

types reflex arcs in ENS

Answer 95

1. simple = single sensory cell, single motor cell - localised 2. complex = simple connected by interneurons - impulse propagated wider

Question 96

main transmitter in ENS

Answer 96

acetylcholine

Question 97

inhibitory transmitters ENS

Answer 97

act on sphincters (these sep sections GI tract) to relax them

Question 98

where do post-gang neurones ANS synapse

Answer 98

parasymp embed in wall GI tract + connect ENS symp = synapse ENS or reduce ACh release at parasymp pre-synapses

Question 99

NTs for ANS digestive sys

Answer 99

all parasymp cholinergic symp pre-gang fibres cholinergic symp post-gang adrenergic (NT noradrenaline)

Question 100

action noradrenaline in symp ANS reponse

Answer 100

* inhibit secretion + motility * decrease blood supply to GI tract

Question 101

entero-enteric reflexes

Answer 101

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*)

Question 102

main regulatory hormones digestive sys + where proded

Answer 102

1. gastrin - stomach 2. secretin - duodenum 3. cholecystokinin (CCK) - duodenum 4. gastric inhibitory peptide (GIP) - SI

Question 103

stim for + effect of gastrin

Answer 103

peptides, aas, Ach HCl production

Question 104

stim for + effect of secretin

Answer 104

HCl pancreatic HCO3-

Question 105

stim for + effect of CCK

Answer 105

FAs, monoglycerides, aas, peptides pancreatic enzs, gall bladder contract

Question 106

stim for + effect of GIP

Answer 106

fat, glucose, aas INHIBITS HCl, STIMS insulin production

Question 107

phases of digestion regulation

Answer 107

1. cephalic 2. gastric 3. intestinal

Question 108

cephalic phase digestive reg

Answer 108

pertains to head, e.g. anticipation food, emotion * coordinated by ANS

Question 109

gastric phase digestive reg

Answer 109

pertains to stomach, e.g. distension, presence peptides * coordinated ANS, ENS, hormones (gastrin)

Question 110

intestinal phase digestive reg

Answer 110

pertains intestins, e.g. distension, lumen contents * coordinated ANS, ENS, hormones (secretin, CCK, GIP)

Question 111

how is appetite regulated

Answer 111

controlled hypothalamus 1. appetite centre causes food searching, direct affect behaviour 2. satiety centre causes refusal food + inhibits appetite centre

Question 112

theories for mechanism appetite regulation

Answer 112

1. glucostat = by levels glucose 2. CCK = by levels CCK 3. lipostat = by levels fat, leptin hormone

Question 113

motility defn

Answer 113

coordinated contraction sm musc in GI tract

Question 114

control contractions GI tract

Answer 114

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

Question 115

how are sm musc contractions in GI tract synchronised

Answer 115

oscillations from pacemaker cells transferred to (+ bet) sm musc via gap junctions

Question 116

leaves greater omentum

Answer 116

1st runs caudally to bladder = superficial leaf then runs cranially my back to the stomach = deep leaf then runs dorsally to body wall

Question 117

limbs pancreas

Answer 117

R runs cranial -> caudal on right, w/in mesoduodenum L runs R -> L across abdomen w/in deep leaf

Question 118

major duodenal papilla

Answer 118

where pancreatic duct empties secretions

Question 119

major duodenal papilla

Answer 119

where pancreatic duct empties secretions

Question 120

structures duodenum

Answer 120

cranial flexure, descending duodenum, caudal flexure, ascending duodenum

Question 121

connecting peritonea duodenum

Answer 121

mesoduodenum -> body wall hepato-duodenal ligament

Question 122

ileal bvs

Answer 122

mesenteric: run parallel to ileum at mesenteric attachment anti-mesenteric: run parallel to ileum on opp side to mesenteric attachment

Question 123

how view hollow GI organs radiograph

Answer 123

feed radio-opaque meal (barium)

Question 124

deglutition

Answer 124

= 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

Question 125

swallowing reflex

Answer 125

press-sensitive sensory cells stimmed + swallowing centre medulla initiates = involuntary

Question 126

how food prevented entering trachea

Answer 126

1. movement food back in mouth forces soft palette up to seal off nasal cavity 2. movement tongue pushes epiglottis shut seal off trachea ## Footnote horse can't breathe thru mouth

Question 127

how does food enter oesophagus

Answer 127

peristalsis = contraction/relaxation muscles

Question 128

what happens in oesophagus

Answer 128

no digestion, just movement food to stomach

Question 129

swallowing disorders

Answer 129

* 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

Question 130

botulism

Answer 130

clostridial toxins block ACh release = can't initiate contractions = can't swallow

Question 131

myaestheania gravis

Answer 131

antibodies formed against ACh receptors = ACh can't bind = no contractions initiated = no swallow

Question 132

anaesthesia relation swallowing

Answer 132

* anaesthetic agents induce vomiting * swallowing process impaired bc reflexes reduced (anaesthetised) = inhalational pneumonia = food/liquid down trachea into lungs

Question 133

oesophagus anatomy

Answer 133

1. mucosal layer stratified squamous = protective inside 2. submucosal layer - bvs + CT 3. muscular layer 4. serosal layer

Question 134

muscular layer oesophagus

Answer 134

* inner circular + outer longitudinal * sk + sm musc * both under involuntary control

Question 135

serosal layer oesophagus

Answer 135

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

Question 136

innervation oesophagus

Answer 136

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

Question 137

after food enters oesophagus

Answer 137

1. upper oesophageal sphincter closes behind bolus so at contraction food no back to mouth 2. epiglottis opens to allow resp 3. peristaltic contractions move food down - inc against gravity, e.g. horse grazing 4. lower oesophageal sphincter opens allow food pass into stomach

Question 138

lower oesophageal sphincter

Answer 138

= cardiac sphincter, seps bottom oes + stomach * physiological sphincter = not anatomically obvious * always closed except in swallowing or gastric acid come up + cause heartburn

Question 139

how is acidic stomach content further prevented re-entering oes

Answer 139

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

Question 140

emesis is + how?

Answer 140

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)

Question 141

how is vomiting controlled

Answer 141

vomiting centre in medulla

Question 142

what stims emesis

Answer 142

* pharyngeal/gastric distension (prevent rupture) * pharyngeal/gastric irritation

Question 143

why can't horses (+ rats) vomit

Answer 143

* lack vomiting reflex * v well developed cardiac sphincter * exaggerated oblique entry oes thru diaphragm | stom usually ruptures b4 vom occurs = stomach tube + suck

Question 144

gastric torsion

Answer 144

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

Question 145

functions simple stom

Answer 145

1. digestion - continuation starch, start prot 2. protection - acid kills bac came w food 3. storage - food delivered SI controlled rate 4. mech breakdown + mix w gastric juices -> semi-liquid **chyme**

Question 146

rumen equiv simple stom

Answer 146

abomasum

Question 147

4 anatomical regions stom

Answer 147

1. cardia = entrance, physiological valve 2. fundus = blind-ending part 3. corpus = bod 4. pylorus = exit

Question 148

cell types in stom mucosa

Answer 148

1. mucous (goblet) - secrete mucus as barrier protect against HCl 2. parietal (oxyntic) - secrete HCl to digest prot 3. chief (peptic) - secrete pepsinogen (inactive form pepsin) to digest prot 4. entero-endocrine - secrete hormones

Question 149

how are cells arranged in mucosa

Answer 149

cylindrical glands

Question 150

why do chief cells secrete pepsinogen

Answer 150

all cells in mucosa etc made up prot so need inactive form pepsin then once reaches stom lumen can be converted to active pepsin

Question 151

role motility in stom

Answer 151

* 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

Question 152

receptive relaxation

Answer 152

initial relaxation stom sm musc when animal starts eating * regulated swallowing centre via vagus * transmitter = vasoactive intestinal peptide

Question 153

motility process in stom

Answer 153

1. starts in fundus - weak contractions, move through 2. propogated down corpus 3. pyloric sphincter opens = chyme -> duodenum 4. contractions reach pylorus = pyloric sphincter closes = food forced back into corpus, helping mixing | MAINLY PERISTALSIS

Question 154

what regs stom emptying

Answer 154

* strength contraction (for how much passes out) * opening/closing pyloric sphincter

Question 155

stimulation stom emptying

Answer 155

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

Question 156

inhibition stom emptying

Answer 156

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

Question 157

topography abdomen

Answer 157

Question 158

digestion offcial defn

Answer 158

enzymatic breakdown nutrient macromols into smaller units that can be absorbed

Question 159

breakdown starch

Answer 159

complex carbs amylose + amylopectin by amylase from saliva (in stom) + pancreas (in SI) @ pH >6

Question 160

hydrolysable carb

Answer 160

can be digested by mammalion enzs - those w α-glycosidic bonds, not w β (= non-hydrolysable)

Question 161

breakdown prot

Answer 161

by pepsin @ low pH

Question 162

how is hydrolysable carb still digested in stom

Answer 162

gradual pH decline from centre stom to edge = amylase stays active for a while

Question 163

comparative starch digestion stom

Answer 163

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

Question 164

comparative salivary amylase levels

Answer 164

* pigs = high * horses = low as diet no usually cont starch * nope in carnivores + ruminants * v high humans as stom not adapted starch digestion

Question 165

main components gastric juice

Answer 165

* HCl * pepsinogen - inactive form pepsin as organs made prot so needs reach stom lumen b4 converted

Question 166

stomach mucosa

Answer 166

v thick layer mucous = protective barrier, v resistant digestion to prevent ulcers

Question 167

functions HCl

Answer 167

* 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

Question 168

secretion HCl process

Answer 168

-> 2-2.5pH

Question 169

alkaline tide

Answer 169

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

Question 170

pepsin working

Answer 170

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

Question 171

auto-catalysis

Answer 171

enz activating own inactive slef

Question 172

stimulation secretion stom

Answer 172

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)

Question 173

cephalic phase stim secretion in stom

Answer 173

neural due sight, smell, taste * direct stim via ACh * indirect stim via gastrin in blood | secretion gastric juice: pepsinogen, HCl, mucous

Question 174

gastric phase stim secretion in stom

Answer 174

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

Question 175

effect food entering duodenum on secretion gastric juice stom

Answer 175

stim or inhib depensing acidity chyme + food components * neural stim (cholinergic) * hormonal stim (gastrin/cholecystokinin) normally inhib

Question 176

role CCK in secretion gastric juices

Answer 176

dogs = partial agonist (low H+) or strong antagonist (high H+) cats = strong agonist

Question 177

hormonal stim release gastric juice

Answer 177

gastrin released blood in response peptides in stom

Question 178

duodenal inhibition secrtion gastric juice

Answer 178

same signals that inhibit stom motility * neuronal via vagus = parasymp * hormonal - secretin, CCK, GIP

Question 179

localised stom inhib gastric juice secretion

Answer 179

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

Question 180

how is stom mucosa protected ulceration

Answer 180

1. secretion thick mucous layer 2. cell mem w interconnecting tight junctions impenetrable by H+ 3. epithelial cells replaced 2-3 days

Question 181

what causes ulcers stom + duodenum

Answer 181

HCl + pepsin damage epithelial cells + underlying tiss: * incr acid prod = duodenal * weakened mucosal layer = gastric damaged cells prod histamine = stims acid secr = worse

Question 182

result ulceration

Answer 182

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

Question 183

pathophysiology

Answer 183

how normal physiology goes wrong

Question 184

causes ulcers

Answer 184

1. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synth - these stim prod mucous + HCO3- so protective mechs reduced 2. mast cell tumours = prod excess histamine = incr HCl prod 3. gastrin-proding tumours = prod excess gastrin = incr HCl prod

Question 185

general idea behind treatment ulcers

Answer 185

1. reduce HCl secr * anti-histamines to block it binding * proton pump inhibitors stop H+ -> gut lumen in secr = less HCl secr 2. protect ulcerated mucosa * antacids neutralise acid * mucosal binding agents bind damaged tiss = protective layer so no further acid damage

Question 186

4 food grps digested where

Answer 186

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

Question 187

absorption

Answer 187

selective process via specific transporter prots by diff down conc grad + 2 AT

Question 188

when are diff substances absorbedin relation body requirements

Answer 188

* organic nutrients + monovalent ions absorbed irrespective body requirements * divalent ions + trace els toxic high concs + absorbed depending body requirements

Question 189

which nutrients absorbed where SI

Answer 189

* most nutrients absorbed entire length * some (B12 + bile salts) only ileum - no transporter prots for them elsewhere

Question 190

phases digestion SI

Answer 190

1. luminal - enzs secreted by salivary glands + pancreas 2. membranous - enzs attached epithelial surface intestinal cells

Question 191

how is SA SI incr

Answer 191

* walls folded = mucosal folds * cells folded = villi * villi folded = microvilli (brush border)

Question 192

intestinal epithelial cell types

Answer 192

1. goblet cells secr mucous - lube + protect - + HCO3- neutralise stom acid 2. Paneth cells defend against microbial penetration 3. eneterocytes responsible absorption via transporter prots = brush border enzs attached for dig 4. enteroendocrine cells control digestion via sensory mechs + release hormones

Question 193

turnover SI cells

Answer 193

migrate from crypts up villus + sloughed off at tip into lumen gut = digested

Question 194

purpose SI motility

Answer 194

1. mix contents w segmental (digestive period) 2. move contents down SI w peristaltic (inter-digestive period)

Question 195

how does SI empty

Answer 195

1. motility stom incr after eating 2. **gastro-ileal reflex** = ileal contractions incr 3. circular musc at ileo-colic junction = physiological valve = sphincter relaxes | to give space for food from stom

Question 196

segmental contractions SI - how work

Answer 196

1. circular contractions along intestine = contents divided segments 2. new contractions in centre distended segment 3. repeated = contents mixed dig juices + moved towards mucosal surface for dig + absorp

Question 197

pattern segmental contractions SI

Answer 197

* 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

Question 198

inter-digestive period

Answer 198

period when dig/absorp complete

Question 199

peristaltic contraction pattern SI

Answer 199

1. irregular moderate activity = short distance + dies out = food no too fast 2. 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

Question 200

how does peristalsis work SI

Answer 200

distension segment = 1. longitudinal musc relax/circ musc contract behind chyme + vice versa in front * motor neurons ENS secr ACh stim contraction sm musc

Question 201

how is contraction type determined

Answer 201

coordination longitudinal + circular musc layers

Question 202

cause contractions SI

Answer 202

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

Question 203

what regs motility SI

Answer 203

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

Question 204

diff bet hydrolysable + non-hydrolysable carbs

Answer 204

α-glycosidic bonds digestble by mammalian enzs β not + requires microbial fermentation

Question 205

carb digestion in luminal phase

Answer 205

* starch -> maltose * salivary amylase continues digestion in stom until acid inhibits * amylase digestion in SI w pancreatic amylase

Question 206

carb digestion membranous phase

Answer 206

enzs attached enterocytes 1. maltose (maltase) -> glucose + glucose 2. sucrose (sucrase) -> glucose + fructose 3. lactose (lactase) -> glucose + galactose | = disaccharidases

Question 207

disaccharidase rate function

Answer 207

maltase + sucrase v fast: Roabsorption limiting factor for how much in blood lactase slower: Rodigestion limiting factor

Question 208

disaccharidase levels varying w age

Answer 208

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

Question 209

how are glucose + galactose absorbed SI

Answer 209

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

Question 210

how is Na+ conc grad maintained gut lumen -> enterocyte

Answer 210

Na+/K+ATPase on basolateral mem * 3Na+ out cell into ISF, 2K+ in * needs ATP = 1AT

Question 211

how is fructose absorbed SI

Answer 211

1. down conc grad -> cell by facilitative transporter GLUT5 = passive 2. down conc grad -> blood via GLUT2

Question 212

what happens to monosacchs once in blood

Answer 212

-> liver via hepatic portal vein: regs everything so toxins removed/detoxed stored as glycogen or in circulation to be metabolised for E

Question 213

do digestive functions adapt to diet

Answer 213

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

Question 214

how is omnivore SI adapted to diet

Answer 214

diet conts high levels hCHO (hydrolysable carb) = SGLT1 levels high throughout

Question 215

how does ruminant SI adapt diet

Answer 215

* SGLT1 expression high lambs: lots lactose milk * rumen develops = less hCHO SI = SGLT1 declines to negligible in adults (down-regulated)

Question 216

how is horse SI adapted diet

Answer 216

SGLT1 highest young, low old but competing fed more hCHO = SI adapts more SGLT1 overall (esp proximally)

Question 217

what causes lactose intolerance + its effects

Answer 217

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

Question 218

prot digestion SI

Answer 218

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

Question 219

absorption products prot digestion

Answer 219

* 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

Question 220

why can't prots be absorbed as intact prot

Answer 220

would be regarded as foreign mat + evoke immune reaction

Question 221

which species have placental transfer maternal antibodies

Answer 221

primates, rodents, dogs, cats | not pigs, ruminants, horses - colostrum

Question 222

how do neonates allow absorption intact antibodies

Answer 222

1. epithelial cells intestine permeable intact prot = holey 2. stom prods negligible amounts HCl 3. pancreatic enz secretion low 4. colostrum conts trypsin inhibitors == no digest antibodies as prot | only 1st 24hrs!!!! then normal function + no more passive immunity

Question 223

relative fat content diff diets

Answer 223

carnivore/omnivore high herbivores low (still have capacity digest)

Question 224

sources fats

Answer 224

triglycerides * plants also have galacto-glycerides + phospholipids * animal tiss conts cholesterol + phospholipids

Question 225

what does lipase breakdown fats to

Answer 225

monoglycerides + free fatty acids (FFAs)

Question 226

where is lipase from

Answer 226

low amounts from saliva/ stom (fat dig starts SI) most secreted in pancreatic juice

Question 227

function bile salts

Answer 227

* 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

Question 228

how do bile salts work

Answer 228

water soluble (neg charge) + fat soluble component * lipid soluble part dissolves in fat droplet * water soluble part protrudes outside fat droplet 1. segmental contractions break fat droplets smaller droplets + neg charges repel so stay as small droplets - no bile = re-coalesce into larger droplets 2. lipase attaches water soluble part emulsified droplet + digests lipids w/in

Question 229

what are micelles + why needed

Answer 229

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

Question 230

metabolism of fat in cells | same for fat soluble vits

Answer 230

1. ER: monoglycerides + FFAs re-esterified form triglycerides 2. coalesce w cholesterol + phospholipids make chylomicrons w prot coat = can be transported lymph + blood (aqueous sol) 3. packaged in G app 4. transferred basolateral mem + released ECF in exocytosis 5. too large enter caps = -> lymph (bypasses liver) -> blood | only nutrient that bypasses liver, otherwise regs all to protect bod

Question 231

absorption water SI routes

Answer 231

1. para-cellular = across tight junctions bet epithelial cells 2. trans-cellular = across cell mem via transporter prots * aquaporins in luminal mem * osmosis thru Na+/glucose or aa transporters (they move thru, water w)

Question 232

effects chylecystokinin

Answer 232

* stims gallbladder contract + release bile * stims release pancreatic enzs * supresses gastric emptying * supresses appetite * triggers peristalsis | all in SI

Question 233

what water is absorbed + where

Answer 233

reabsorption digestive juice secretions + water from food mostly SI, some LI more maximum reabsorption to prevent dehydration | horses = most water absorption in LI

Question 234

how is Na+ absorbed

Answer 234

via many transporters to provide E for 2AT

Question 235

how are K+ + Cl- absorbed

Answer 235

diffusion, usually associated w other ions, e.g. Na+

Question 236

how is bicarbonate absorbed + why

Answer 236

lost secreted in digestive juices SI so need reabsorb prevent metabolic acidosis * HCO3-/Cl- counter transporter

Question 237

how is H3PO4 absorbed

Answer 237

* 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

Question 238

function phosphate in gut

Answer 238

* rumen buffer w HCO3- to maintain pH * important source nutrition ruminal microbes

Question 239

how is iron absorbed

Answer 239

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

Question 240

how is Ca2+ absorbed

Answer 240

1. passive transport - high dietary incr rate 2. 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

Question 241

functions LI

Answer 241

* absorption water + ions * fermentation non-hydrolysable carbs - degree depends amount fibre diet - loads horses, no carnivores, some ruminants

Question 242

what do glands mucosa LI secrete

Answer 242

* mucous for protection/lubrication * HCO3- to neutralise VFAs | only microbial digestion so no digestive enzs

Question 243

which part colon varies bet species + how

Answer 243

ascending colon: * simple carnivores * omnivores/ruminants = moderate * horses = extensive

Question 244

rectum

Answer 244

terminal part colon for storage faeces b4 egestion

Question 245

main cell types LI

Answer 245

1. colonocytes = absorptive but no villi, just crypts (invaginates lining) + less microvilli - less absorption so smaller SA 2. goblet cells: mucous + HCO3- for lubrication hard stuff in lumen (water absorbed)

Question 246

fermentation

Answer 246

of fibre by microbes -> volatile FAs (VFAs) = E source as absorbed (not wanted by microbes)

Question 247

role VFAs

Answer 247

1. E source 2. maintain homeostasis colonic epithelium by regulating genes controlling proliferation, apoptosis, differentiation

Question 248

main VFAs

Answer 248

1. acetate - used liver, oxed other cells to gen ATP, source acetyl CoA for lipid synth 2. propionate = substrate gluconeogenesis 3. butyrate = E production, cellular homeostasis so not enough fibre = more prone colon cancer

Question 249

how are VFAs absorbed LI | VFAs = short chain FAs (SCFAs)

Answer 249

absorbed by SCFA/HCO3- exchanger

Question 250

how is Na+ absorbed LI

Answer 250

Na+ channs + Na+/H+ exchanger - enhanced by aldosterone

Question 251

how is Cl- absorbed LI

Answer 251

bicarbonate/hydroxyl exchange

Question 252

how is water absorbed LI

Answer 252

* 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

Question 253

diarrhoea is?

Answer 253

water lost in faeces thru incr secretion + decr absorption * incr water content = distension = incr motility = absorption further reduced

Question 254

causes diarrhoea

Answer 254

1. nutritional, e.g. change composition diet too fast = gut can't absorb (wrong enzs) = osmotic flow water into gut lumen 2. infections, e.g. E. Coli bac secrete enterotoxins bind cell mem epithelia stimming cAMP in glands = hyper-secretion 3. stress = strong activation parasymp sys = incr secr + motility

Question 255

how to treat diarrhoea

Answer 255

* 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

Question 256

contractions in LI

Answer 256

1. segmental in caecum/colon, lower frequency than SI 2. peristaltic 3. anti-peristaltic, most prominent proximal colon w mat back to caecum 4. mass movement, only in LI towards rectum for evac

Question 257

intrinsic regulation motility

Answer 257

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

Question 258

extrinsic reg motility

Answer 258

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

Question 259

what is constipation

Answer 259

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

Question 260

how do we treat constipation

Answer 260

* oral fluids to soften faecal mat * non-digestible mat like paraffin oils to lubricate * drugs to strengthen contractions - usually enemas

Question 261

how do we defaecate

Answer 261

1. press sensitive cells in rectum stim defaecation reflex 2. terminal colon + rectum contract 3. inner anal sphincter sm musc relaxes 4. 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

Question 262

structure exocrine pancreas

Answer 262

* grps acini (clusters epithelial cells) * simple cuboidal epithelium around excretory duct * lots ducts combine to pancreatic/accessory pancreatic duct

Question 263

structure endocrine pancreas

Answer 263

isolated clumps cells around capillary = islets of Langerhans

Question 264

functions pancreas

Answer 264

1. digestion (exocrine) -> dig enzs + bicarbonates neutralise stom acid = protect intestinal mucosa + provide pH enzs work 2. reg metabolism (endocrine) -> insulin + glucagon

Question 265

relative amounts pancreatic juice proded diff species

Answer 265

horse/pig = lots for suitable intestinal environ for fermentation * equiv saliva production ruminants

Question 266

ionic composition pancreatic juice

Answer 266

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)

Question 267

how is alkaline tide negated

Answer 267

H+ transported bloodstream from pancreatic duct when water blood -> duct (osmosis) = blood normal

Question 268

which dig enzs secreted by pancreas

Answer 268

1. proteases secreted inactive form prevent autodigestion (pancreas made up prot) - trypsin(ogen), chymotrypsin(ogen), (pro)elastase, (pro)carboxypeptidase 2. amylase to break down starch 3. lipases/phospholipases fat -> glycerol/FAs 4. ribo/deoxyribo-nuclease break down RNA/DNA

Question 269

how are proteases activated from pancreas

Answer 269

1. duodenal epithelial surface conts enteropeptidase: trypsinogen -> trypsin 2. trypsin autocatalyses itself + activates other proteases pancreatic cells prod trypsin inhibitor = precaution against autodigestion

Question 270

which dig phases cause pancreatic juice secretion

Answer 270

all 3

Question 271

how do dig phases reg pancreatic secretion

Answer 271

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

Question 272

how does secretin work

Answer 272

released from duodenum in response H+ + incr HCO3- secr = neg feedback mech (as acid neutralised stim for secr decr)

Question 273

how does cholecystokinin work

Answer 273

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....)

Question 274

diffs in pancreatic secr bet species

Answer 274

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

Question 275

why is horse pancreatic juice diff

Answer 275

low HCO3- = only able neutralise acidic stom contents bc ileum secretes loads HCO3- (also neutralises VFAs from fermentation in LI

Question 276

types cells in islets Langerhands + which hormones prod

Answer 276

1. β -> insulin 2. α -> glucagon 3. δ (delta) -> somatostatin, inhibits insu + gluca (paracrine so only has effect in area secreted) = pancreas self-reg

Question 277

where are pancreatic hormones proded + where go

Answer 277

secreted in bloodstream -> liver (via hepatic portal vein) -> other tissues to effect

Question 278

how + why is insulin proded

Answer 278

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

Question 279

reg insulin locally

Answer 279

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

Question 280

how does ANS reg insulin secr

Answer 280

parasymp activity (via vagus) = incr secr from long-reflex arc symp activity+ adrenaline = decr secr

Question 281

insulin action target cells

Answer 281

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

Question 282

what metabolism is caused by insulin + where

Answer 282

* 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

Question 283

diabetes mellitus

Answer 283

plsma gluc incr (hyperglycaemia) bc decr cell uptake = kidney capacity reabsorb gluc exceeded (glucosuria)

Question 284

types diabetes

Answer 284

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

Question 285

what causes IDDM

Answer 285

* pancreatic inflammation * hypersecretion hormones antagonistic to insulin (cortisol, growth hormone) * obesity

Question 286

hyperglycaemia results in?

Answer 286

* 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

Question 287

polyuria

Answer 287

excessive urine vol

Question 288

polydipsia

Answer 288

excessive thirst

Question 289

hypoglycaemia

Answer 289

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

Question 290

glucagon production

Answer 290

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

Question 291

glucagon action

Answer 291

1. stimmed by decr plasma glucose + incr plasma aas (substrate for gluconeogenesis) + incr symp activity 2. binds receptors on target cells to activate adenyl cyclase 3. acts opp insulin w net effect dependent ratio 4. incr plasma gluc by stimming liver glycogenolysis + gluconeogenesis (substrate propionate VFA + aas)

Question 292

why is liver lobated/not

Answer 292

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

Question 293

overall cellular structure

Answer 293

liver surrounded capsule CT that extends into liver as v branched septae * septae create structural units = hepatic lobules around central vein (hexagonal)

Question 294

functional cells liver

Answer 294

hepatocytes

Question 295

how do hepatocytes absorb

Answer 295

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

Question 296

how biliary sys works

Answer 296

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'

Question 297

function gall bladder

Answer 297

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)

Question 298

blood in + out liver

Answer 298

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

Question 299

how does blood mix in liver + where does it go inside

Answer 299

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

Question 300

where are vessels located in liver structure

Answer 300

portal tracts (triads) bile duct, hepatic artery + portal vein bet lobules then blood goes into liver down sinusoids to central vein

Question 301

hepatic acinus

Answer 301

functional unit liver * liver in zones corresponding distance arterial blood supply (from O2 supply) * zone 1 = closest * pattern death inwards from zone 3

Question 302

endothelium + contents sinusoids

Answer 302

* fenestrated for mols enter hepatocytes * Kupffer cells = macrophages to patrol + destroy

Question 303

general function + what stuff goes where

Answer 303

blood in sinusoids 1. bad stuff -> hepatocytes -> bile duct 2. normal stuff stays -> central vein

Question 304

functions liver

Answer 304

1. detox body waste, drugs 2. synth cholesterol + bile acids

Question 305

# [](http://) what's in bile

Answer 305

* bile acids = digestive component * waste for excretion

Question 306

functions hepatocytes

Answer 306

* synth plasma prots * breakdown rbcs * carb, lipid + aa metabolism * removal bac * production clotting factors * storage glycogen, Fe, Cu, vits

Question 307

carb metabolism in liver

Answer 307

* glycogenesis * glycogenolysis * gluconeogenesis (maintain blood gluc)

Question 308

lipid metabolism in liver

Answer 308

* oxidation FAs + ketone body formation * synth cholesterol, phospholipids, bile acids

Question 309

prot metabolism in liver

Answer 309

* deamination + transamination aas * synth non-essent aas

Question 310

what does liver do to toxins

Answer 310

generic phase: coenz cytochrome P450 oxidises specific phase: further degradation -> aas, sulfate -> urinary/biliary sys | = conversion to less toxic compounds

Question 311

which things detoxed in liver

Answer 311

1. drugs 2. toxins 3. endogenous metabolites - NH3 from prot breakdown, hormones once done, haem

Question 312

example plant toxin

Answer 312

digitalis from foxglove = heartbeat faster + stronger

Question 313

degradation of rbcs

Answer 313

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

Question 314

what makes urine yellow

Answer 314

in intestines conjugated bilirubin -> urobilinogen (yellow) -> kidney

Question 315

layers of lining GI tract | inside to outside

Answer 315

1. mucosa = mucous epithelium -> lamina propria -> muscularis mucosae (sm musc, no in rumen) 2. submucosa = loose CT w bvs, nerve plexuses 3. muscularis = circular (inner) + longitudinal (outer) 4. serosa = CT layer + peritoneum

Question 316

what are papillae

Answer 316

small outgrowths dorsal surface tongue * filiform = long, threadlike * circumvallate + fungiform = cushion-shaped * foliate = succession of folds keratinised stratified squamous epithelium studded w tastebuds

Question 317

how does mucosa change down GI tract

Answer 317

1. stratified squamous oesophagus w mucous glands 2. thicker, folded in stom w mucous glands, parietal cells (in lamina propria), simple columnar 3. pyloric region = less chief + parietal + gastric glands to start buffering acid for duoden 3. way way thicker single layer epithelium on v long villi duoden 4. jejunum = villi get more slender 4. ileum = villi get shorter 5. colon = more even thickness w loads goblet cells for loads mucus move stuff along, now even sized colonic crypts not villi

Question 318

how does muscle type change down GI tract

Answer 318

sk in oesophagus -> sm * dogs = changes at oesophagus stom junction * pigs = as passes thru diaphragm * horses = @ caudal 1/3 oesophagus

Question 319

Brunner's glands

Answer 319

secrete alkaline mucous in duoden (found submucosa) to protect from stom acid

Question 320

what distinguishes ileum lining from rest GI tract

Answer 320

Peyer's patches = lymphoid associated tiss (so purple w H&E bc lymphocytes)

Question 321

reticulum inner lining

Answer 321

papillae w muscularis mucosae extending into it - arranged honeycomb appearance - + keratinised stratified squamous

Question 322

where is ENS located

Answer 322

nerve plexuses bet inner + outer muscularis layers + smaller plexuses in submucosa

Question 323

purpose muscularis mucosae

Answer 323

sm musc to keep epithelium in contact w lumen contents + allow contents glands empty out

Question 324

bile functions

Answer 324

1. emulsify lipids so accessible pancreatic lipases 2. makes micelles so lipids soluble + intestine can uptake 3. exit route waste products, drugs, excess cholesterol

Question 325

components bile

Answer 325

* water * electrolytes - HCO3- makes it alkaline * biliary prots * bile pigments * cholesterol * phospholipids * bile acids

Question 326

synth + development bile acids | from x to y .... thru GI tract

Answer 326

Question 327

how are bile acids secreted

Answer 327

1. AT into bile canaliculus by transporter prot Bile Salt Excretory Pump (BSEP) - canaliculi isolated hepatocytes mem w tight junctions so no leakage 2. canaliculi feed into large canals 3. emptied into duodenum at major duodenal papilla, controlled Sphincter of Oddi (sm musc contracts circularly) 4. not fat soluble = stay in SI until ileum where transport prots reabsorption | or goes gall bladder for storage + later release

Question 328

enterohepatic circulation

Answer 328

1. bile acids reabsorbed AT terminal ileum 2. transported in hepatic portal vein -> liver 3. captured from bloodstream via Na+-dependent Taurocholate Co-transporting Polypeptide (NTCP) 4. recycled (95%)

Question 329

how is bile secretion regulated

Answer 329

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

Question 330

sphincter of oddi in animals w/o gall bladder

Answer 330

inactive so constant flow bile into duoden - horses constantly eating

Question 331

causes liver disease + problems

Answer 331

infection, poisoning, tumours affects bile acid recycling, detoxification, metabolic functions | liver can regenerate so some disease reversible

Question 332

clinical signs liver disease

Answer 332

* 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)

Question 333

incr/decr liver size

Answer 333

incr = hepatomegaly decr = microhepatica

Question 334

liver enzs released when liver damaged

Answer 334

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

Question 335

how measure liver function

Answer 335

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

Question 336

cholestasis

Answer 336

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

Question 337

porto-systemic shunts are?

Answer 337

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

Question 338

clinical signs porto-systemic shunts

Answer 338

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

Question 339

methods diagnosis porto-systemic shunts

Answer 339

* ultrasound * fluoroscopy = x-rays thru bod over period time to get video movements inside * exploratory laparotomy = find bvs + see if connected

Question 340

exocrine gland

Answer 340

secretes products into duct that delivers to lumen of organ or free surface of epithelium (e.g. skin)

Question 341

endocrine gland

Answer 341

secfetes product into extracellular space where quickly taken up by blood | no duct

Question 342

zymogen granules

Answer 342

in pancreatic acinar (exocrine) cells - where enzs + proenzs stored before release | stain brightly

Question 343

what do serous cells pancreas secrete

Answer 343

isotonic fluid cont (pre)enzs, enz inhibitors + HCO3- * by exocytosis into duct = merocrine

Question 344

microscopic structure exocrine pancreas/salivary duct | v similar

Answer 344

* 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

Question 345

how are endocrine + exocrine arranged in pancreas

Answer 345

islets Langerhans (endocrine) scattered thruout lobules exocrine tiss (majority, 80%) | endocrine stained a bit lighter + near caps for hormones enter

Question 346

which salivary glands secrete which saliva types

Answer 346

parotid = serous (w enzs, bicarb etc in) mandibular, buccal, sublingual = mix mucous + serous

Question 347

serous vs mucous saliva in simple-stomach vs complex stomach animals

Answer 347

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

Question 348

purpose myoepithelial cells in salivary gland

Answer 348

contract to squeeze saliva from duct upon nerve stim

Question 349

ito cells

Answer 349

== stellate cells in space of Disse * store vit A - visible vacuole cont lipid

Question 350

direction bile flow

Answer 350

opp from direction blood flow * duct runs from near central vein to portal triad w portal vein + hepatic artery

Question 351

gall bladder epithelium

Answer 351

* simple columnar lining * v vascular lamina propria * external musc layer of randomly oriented sm musc * **folded** so can expand + retract as required

Question 352

absorptive + post-absorptive state

Answer 352

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

Question 353

what happens in absorptive state

Answer 353

1. cells use nutrients source E + prot synth 2. galactose/fructose converted glucose in liver 3. liver fills glycogen stores + synths lipids for export other tissues 4. excess carb, fat, prot stored as lipid/glycogen (sk musc = glycogen storage) 5. all cells net synth prot ruminants = carb fermented to VFAs - don't absorb glucose intact | lipid not as efficient as glucose at releasing E

Question 354

what happens to glucose in liver

Answer 354

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

Question 355

what happens glucose in adipose tiss

Answer 355

taken up + converted glycerol for synth triglycerides as reserve source E * excess = some converted FFAs | its the FFAs taken up

Question 356

how are lipids made water soluble for transport in blood

Answer 356

binding to prots 1. FFAs bound albumin 2. others bound apoprots = lipoprots apoprots = interface bet lipid core + aqueous environ = can be transported

Question 357

types lipoprot + where transport lipids

Answer 357

1. chylomicrons = fat absorbed GI tract -> rest bod 2. VLDL = synthed liver -> elsewhere 3. LDL = synthed liver from VLDL -> transport cholesterol other cells 4. HDL = synthed liver, transports apoprots for lipid uptake, then cholesterol -> liver | very low/low/high density lipoprot

Question 358

what happens chylomicrons + VLDL

Answer 358

1. converted FFA by lipoprotein lipase in cap wall 2. taken up adipose tiss (stored as triglycerides)/ musc (oxed for E) 3. remnants taken up by liver + metabolised 4. remaining VLDL remnants converted LDL - transfer cholesterol -> cells

Question 359

when can musc metabolise lipids

Answer 359

in aerobic environ - FFAs

Question 360

why do cells need cholesterol

Answer 360

lil bit to make phospholipid mems

Question 361

what does HDL do

Answer 361

* apoprots -> chylomicrons + VLDL, incr lipid uptake * remove cholesterol cells + transfer liver = cholesterol-rich HDL - degraded release cholesterol converted bile salts/excreted in bile

Question 362

what happens aas absorbed

Answer 362

* 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

Question 363

role keto acids

Answer 363

* provide E liver cells (Krebs cycle) * converted glucose/glycogen * converted FAs for lipid synth * used synth non-essential aas

Question 364

what happens to degraded aas

Answer 364

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

Question 365

how does bod provide E in post-absorptive state

Answer 365

* 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)

Question 366

how is post-absorptive state requirements different in pregnancy/lactation

Answer 366

glucose essential (other sources no se va) for foetal metabolism + lactose syth == maintenance plasma glucose levels extra important

Question 367

how does liver respond reducing plasma glucose levels

Answer 367

1. reduces anabolic activities (overall activity) 2. mobilising glycogen stores to release glucose (only sufficient maintain few hrs)

Question 368

gluconeogenesis

Answer 368

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

Question 369

sk musc in post-absorptive state

Answer 369

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

Question 370

what happens FFAs in post-absorptive state

Answer 370

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

Question 371

what happens FFAs taken up by liver

Answer 371

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

Question 372

alternative source ket bods ruminants + why important

Answer 372

synthed from VFA butyrate in epithelial cells - v important bc butyrate inhibits gluconeogenesis | ketosis if levels ket bods too high

Question 373

what regs carb metabolism

Answer 373

1. insulin - incr uptake gluc, stim glycogenesis, incr gluc use, inhibit gluconeo 2. glucagon opp 3. adrenaline 4. glucocorticoids have role in gluconeogenesis

Question 374

effect adrenaline in carb metabolism

Answer 374

* 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)

Question 375

regulation prot metabolism

Answer 375

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

Question 376

regulation fat metabolism

Answer 376

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

Question 377

when does gluconeogenesis occur ruminants

Answer 377

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

Question 378

where does fermentation occur diff species

Answer 378

carnivores = small degree stom omnivores = lil bit LI herbivores = fore-stom or LI (= hindgut fermenters)

Question 379

fermentation

Answer 379

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

Question 380

what happens to stuff from fermentation in fore-gut fermenters

Answer 380

* VFAs (fermentation produucts) absorbed in stom * microbial prot passes abomasum + SI for dig + absorp = main source prot

Question 381

what happens stuff from fermentation hindgut fermenters

Answer 381

LI = fermentation chamber * VFAs absorbed in colon * microbial prot lost faeces - rabbits do coprophagy (eat poop)

Question 382

fore-gut vs hindgut fermentation

Answer 382

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)

Question 383

ruminant nutritional strategies

Answer 383

1. browsers (concentrate selectors), e.g. deer = select fruit, seeds, buds high hydrolysable carb (simple sugars) 2. grazers (grass/roughage eaters), e.g. cow = eat fibrous 3. intermediates (adaptable feeders), e.g. goats

Question 384

simple sugars vs VFAs as source E

Answer 384

simple sugars more efficient source E

Question 385

browser vs grazer adaptations | in a table

Answer 385

Question 386

oesophageal/ventricular groove

Answer 386

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

Question 387

what happens if cold milk suckled

Answer 387

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

Question 388

dig enzs diff species types

Answer 388

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

Question 389

where is stuff absorbed diff species

Answer 389

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

Question 390

deglutition

Answer 390

swallowing

Question 391

regurgitation

Answer 391

passive transfer stom contents to oral cavity for remastication

Question 392

re-mastication

Answer 392

additional chewing fibrous mat that was regurgitated

Question 393

rumination

Answer 393

process re-gurgitation, re-mastication, re-deglutition

Question 394

adaptation rumen stom + structure

Answer 394

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

Question 395

where does fermentation occur ruminants

Answer 395

fore-stom (most) + LI (anything that escaped in rumen)

Question 396

overall strcuture reticulum + rumen | diagram from left side

Answer 396

Question 397

reticulum structure

Answer 397

* inner surface raised into ridges (honeycomb) * wall lots sm musc | 10-20L capacity

Question 398

rumen structure

Answer 398

* 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

Question 399

histology fore-stom wall

Answer 399

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

Question 400

omasum function + structure

Answer 400

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

Question 401

structure abomasum

Answer 401

columnar epithelium w glands 1. HCl 2. pepsinogen 3. rennin (young) to precipitate casein (milk prot) + retain milk longer for pepsin act

Question 402

regulation movement stuff -> + out of abomasum

Answer 402

receives constant flow fermented mat from omasum * distension inhibits rumino-reticular contractions = flow slows * regulation emptying same as simple stom

Question 403

how is abomasum pH diff from simple stom

Answer 403

pH slightly higher due alkilinity fermentation fluid * still acidic - kill bac, ruminal microbes for digestion

Question 404

where are digestive components distributed

Answer 404

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

Question 405

types rumino-reticulum contractions

Answer 405

1. primary (mixing contents) 2. secondary (eructation) 3. rumination

Question 406

how many primary ruminal contractions should there be at diff stages eating

Answer 406

EATING: 5-8 strong contractions/5mins RUMINATING: 4-5 contractions/5mins FASTING: 0-1 weak contractions/5mins

Question 407

how often do secondary ruminal contractions occur

Answer 407

after every 2-3 primary contractions

Question 408

process primary rumino-reticulum contractions

Answer 408

1. 1st reticular = coarse mat -> central/dorsal rumen 2. 2nd reticular = fermented mat -> cranial blind sac + small vol (50-100ml) fermented mat thru reticulo-omasal orifice -> omasum 3. cranial blind sac = moderately fermented mat -> dorsal sac + well fermented -> reticulum 4. dorsal sac = backwards contraction (caudal -> cranial) w overall circular movement contents in dorsal sac + some exchange w ventral sac 5. ventral sac = backwards w overall circular movement contents ventral sac (fine mat), some exchange w dorsal + well-fermented -> cranial blind | thing named contracts

Question 409

rumination contractions when + why

Answer 409

occurs when coarse mat stims oesophageal opening * extra reticular contraction then normal primary * occurs when resting after eaten | ruminants have to ruminate

Question 410

process rumination contraction

Answer 410

1. newly swallowed mat forced -> dorsal sac + replaced partially fermented mat (that's what goes back up) 2. thorax expands, gening neg press in thorax 3. lower oesophageal sphincter opens 4. diaphragmatic musc contracts = forces mat into oes (NOT abdominal wall muscs) 5. antiperistalsis in oes = food -> oral cavity 6. liquid immediately reswallowed 7. rest mat rechewed w extra salivary secretion + reswallowed

Question 411

why require secondary contractions

Answer 411

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

Question 412

eructation process | (secondary contractions)

Answer 412

1. caudal-dorsal blind sac contracts forward = contents -> cranial blind sac + ventral sac 2. dorsal sac conts contracting = gas at top -> oesophageal opening 3. incr neg press in thorax = oes expands 4. cardiac sphincter opens + gas -> oes, antiperistalsis = -> oral cavity 5. some escapes via mouth, most inhaled 6. ventral sac contraction = gas collecting in caudo-ventral sac blind sac escape -> top dorsal sac | after every 2-3 primary contractions

Question 413

bloat causes

Answer 413

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)

Question 414

results of bloat

Answer 414

* incr ruminal press = respiratory + cardiac distress * stretching rumen reduces/stops rumen contractions (mechanoreceptors)

Question 415

what regs fore-stom motility

Answer 415

mainly autonomic long reflexes - afferent + efferent fibres in vagus (= vago-vagal reflex) * tension, mechano + chemoreceptors play off to reg

Question 416

stimulation + inhibition rumen motility

Answer 416

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**

Question 417

result increased motility

Answer 417

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

Question 418

result decr motility

Answer 418

rumination decr = food particles broken down more slowly = decr rate passage food

Question 419

where is rumen motility controlled

Answer 419

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

Question 420

GI situation at birth + initial development after

Answer 420

1. abomasum developed but not fore-stom 2. fore-stom developed when starts eat roughage (2-3wks) 3. lamb dependant milk for nutrition + microbes for fermentation received from mother as licks

Question 421

microbial fermentation

Answer 421

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

Question 422

what is retained longest in rumen

Answer 422

lignified roughage retained longer than succulent herbage bc harder breakdown - needs longer to be fermented

Question 423

why rumen anaerobic

Answer 423

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

Question 424

how is rumen made anaerobic

Answer 424

facultative anaerobes = anaerobic bac + can use O2 - adhere luminal surface + remove all O2

Question 425

micro-organisms present in rumen

Answer 425

bac = amylolytic (ferment hydr carb) + cellulolytic (non-hydr) protozoa fungi

Question 426

how long are diff microbes retained rumen

Answer 426

1. amylolytic bac short lifespan + exist fluid phase = ejected w contents 2. cellulolytic bac/protozoa/fungi longer lifespan = need stay longer to establish, proliferate, work = attach luminal wall or fibre

Question 427

how is sterile rumen made microbial

Answer 427

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

Question 428

types bac in rumen

Answer 428

1. amylolytic = hydr carb, break α-glycosidic -> monosacchs - high tolerance low pH + can proliferate fast 2. cellulolytic = cellulose, hemi-cellulose, fructosans, pectin, break β-glycosid -> monosacchs - low tolerance low pH 3. proteolytic = prot -> peptides -> aas for microbial prot synth/fermentation -> VFAs + NH4+ 4. methanogenic = CO2 -> CH4 5. lactate-utilisers = lactate -> propionate

Question 429

protozoa in rumen

Answer 429

1. prod VFAs, lactate, CO2 + H2 2. 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

Question 430

fungi in rumen

Answer 430

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

Question 431

homeostasis rumen environ

Answer 431

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

Question 432

how does rumen acidosis happen

Answer 432

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

Question 433

how treat rumen acidosis

Answer 433

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

Question 434

what determines Rofermentation

Answer 434

* feedstuff type - starch fermented more rapidly than fibre * vol feedstuff * microbial balance - amylolytic bac ferment faster than cellulolytic

Question 435

why are fore-gut fermenters more resitant to toxins than hind-gut

Answer 435

rumen microbes can degrade toxins before absorption = can cope w higher levels before problem | e.g. foxglove, ragwort

Question 436

carb metabolism ruminants

Answer 436

1. bac surface enzs break down -> monosacchs/short-chain polysacchs 2. dissolved rumen fluid + taken up microbes + metabolised (glycolysis) to provide E for microbes 3. anaerobic so glycolysis only -> VFAs 4. waste product for microbes but source E for ruminants 5. propionate from anaerobic glycolysis pyruvate + from lactate | diet high starch = more lactate-utilisers = more VFA AND more propionate

Question 437

why prod methane

Answer 437

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

Question 438

how else can NAD+ be regened in rumen

Answer 438

reduction sulphate/nitrates by other ruminant bac

Question 439

how is fat metabolised rumen

Answer 439

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)

Question 440

why does ruminant body fat differ other species

Answer 440

unsaturated FAs synthed as stereoisomeric cis form in animal tiss but ruminal bac hydrogenation also gens some trans unsaturated FAs

Question 441

how is prot metabolised rumen

Answer 441

degraded by ruminal bac -> * peptides * aas * NH3 + organic acids * branched FAs

Question 442

rumen microbial proliferation

Answer 442

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

Question 443

what is NPN w examples

Answer 443

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)

Question 444

how is NPN metabolised

Answer 444

microbes: NPN -> NH3 -> aas -> prot microbial prot digested stom/SI as in simple stom

Question 445

why do we need NPN + examples good sources

Answer 445

essential healthy microbial pop * grass/grain 5-15% * silage 70% (due microbial fermentation)

Question 446

extra prot dairy cow diet | bc require more when lactating than from NPN

Answer 446

1. urea added to incr NPN = incr microbial pop - need more E to proliferate (usually form hCHO, e.g. molasses) 2. '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

Question 447

what happens surplus prot ruminants

Answer 447

recycled into urea (liver) + secreted saliva excess urea excreted kidneys = E costly so don't overshoot NPN in diet

Question 448

absorption defn

Answer 448

selective transfer useful nutrients into host's bloodstream

Question 449

absorption in rumen

Answer 449

* 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

Question 450

which parts rumen permeable what

Answer 450

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

Question 451

what happens to VFAs as absorbed

Answer 451

1. acetic acid absorbed unchanged 2. some propionic acid metabed -> lactic acid 3. all butyric acid -> β-hydroxybutyric acid

Question 452

what happens to water in rumen

Answer 452

moves bet rumen + ECF depending osmotic grad

Question 453

what happens lactic acid in rumen

Answer 453

stronger acid = more poorly absorbed than VFAs = remains rumen lowering pH * when absorbed liver converts -> glucose

Question 454

what happens NH3 in rumen

Answer 454

rapidly absorbed so equilibrium constantly shifting so NH4+ -> NH3 * absorbed = converted -> urea by liver

Question 455

inorganic ion movement bet rumen + blood

Answer 455

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

Question 456

what happens in omasum as passing -> abomasum

Answer 456

* 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

Question 457

omasal canal

Answer 457

allows mat pass straight rumen -> abomasum

Question 458

parts colon in horse

Answer 458

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)

Question 459

muscle in horse LI

Answer 459

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

Question 460

how much fermentation in LI diff species

Answer 460

CARNIS: most dig/absorp already done = minimal fermen RUMIS/OMNIS: moderate HORSES: most non-hydr carb -> LI so extensive

Question 461

what happens products fermentation horses

Answer 461

VFAs absorbed LI muscosa -> blood gases CH4 + CO2 -> rectum (peristalsis) + expelled (flatulence) | last stage so some VFAs + all microbial prot wasted

Question 462

metabolism + role VFAs horse

Answer 462

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

Question 463

how are VFAs absorbed horse

Answer 463

SCFA/HCO3- exchanger in LI

Question 464

how is Na+ absorbed horse

Answer 464

Na+ channs + Na+/H+ exchanger in LI * enhanced by aldosterone

Question 465

how is Cl- absorbed horse

Answer 465

bicarbonate or hydroxyl exchange in LI | maintains pH at suitable level fermentation

Question 466

water absorption horses

Answer 466

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)

Question 467

benefit horse dig sys compared ruminants

Answer 467

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

Question 468

fibre fermentation + response horses | + what happens when fails

Answer 468

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

Question 469

difference prot fermentation horses compared ruminants

Answer 469

equine hindgut more capable absorbing aas/peptides = less taken up by microbes = good bc microbial prot lost

Question 470

how are microbial N requirements met horse

Answer 470

urea secreted by ileum/LI -(microbial urease)> NH3 = NPN source microbial prot synth

Question 471

difference in how prots absorbed horse vs ruminant

Answer 471

absorbed intact not metabed as absorbed * so prop propionic acid for gluconeogenesis incr w incr hCHO -> LI

Question 472

diffs in microbes present horse LI compared rumen

Answer 472

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

Question 473

how + why caecum diff in horses

Answer 473

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)

Question 474

caecal contractions horse

Answer 474

1. segmental = high microbial activity = high fermen + absorp 2. mass so all -> colon every 3-5mins = sm musc whole caecum contracts longer

Question 475

colon contractions most species

Answer 475

1. segmental + peristaltic 2. anti-peristaltic prominent proximal colon 3. chyme colon -> caecum 4. mass descending -> rectum (+ out caecum)

Question 476

colonic contractions horse different how?

Answer 476

* 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)

Question 477

equine colic

Answer 477

= 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

Question 478

normal sounds/locations horse auscultation

Answer 478

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

Question 479

abnormal sounds abdominal auscultation horse

Answer 479

1. incr frequency = enteritis/ spasmodic colic (SI overdrive, sm musc relaxant) 2. tympanitic = hollow, drum-like = gut distension w gas = obstruction 3. decr frequency = ileus (surgeon handles guts + stop working)/obstruction (can't get thru = movement slowed)

Question 480

normal rectal exam horse | diagram

Answer 480

Question 481

rectal exam if SI obstruction

Answer 481

surgical colic = needs referral

Question 482

rectal exam ileal impaction

Answer 482

= blocked as going into caecum * don't feel SI distension if catch early

Question 483

rectal exam caecal impaction

Answer 483

PRIMARY = impaction w ingesta SECONDARY = due obstruction large colon

Question 484

rectal exam colonic impaction

Answer 484

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)

Question 485

impaction defn

Answer 485

blockage, abnormal accumulation food mat

Question 486

rectal exam: left dorsal displacement

Answer 486

== 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

Question 487

rectal exam: right dorsal displacement

Answer 487

large colon lateral to caecum

Question 488

torsion vs volvulus

Answer 488

torsion = twisting of organ round its own axis volvulus = twisting of organ round axis perpendicular to own

Question 489

rectal exam: large colon volvulus/torsion

Answer 489

volvulus 1st but often associated w torsion * then all abdo bvs trapped = no blood back heart = hypovolaemic shock

Question 490

rectal exam: small colon impaction

Answer 490

Question 491

how identify spinal nerves

Answer 491

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

Question 492

tight + loose stom attachments

Answer 492

1. greater omentum = loose (folds etc) 2. lesser omentum = tight to liver _ liver firmly attached diaphragm = no movement 3. gastro-splenic ligament = tight but spleen no attached = can move w stom 4. tightly attached oes | stom can't move much, only really rotate: normally volvululs

Question 493

why extra doubly shouldn't handle pancreas

Answer 493

handle = damage damage a cell = releases its contents pancreas cells cont loads proteases = cells break down = much more discomfort than damage other organs

Question 494

how distinguish bet 3 parts SI

Answer 494

1. duoden only one w Brunner's glands to secr mucous 2. ileum only one w Peyer's patches as part IS 3. jejunum has neither 1. jejunum = bvs hit at right angles 2. ileum = bvs run along its length

Question 495

purpose caecum

Answer 495

reserve space = slow digestion colon w reserve space w/o distension or food returning ileum

Question 496

why so many diff bvs to each organ

Answer 496

in normal movement if right side squished + bvs squished blood supply to that organ still continues

Question 497

what is CT scan

Answer 497

radiography but lots images put together make 3D image

Question 498

what are MRI scans used for

Answer 498

mostly looking at nervous sys | v expensive

Question 499

why ultrasonography no good for looking at GI sys

Answer 499

too much motility = can't really see