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Liv vet med yr1 > GI > Flashcards

GI Flashcards

1
Q

Composition of saliva

A

Dependent on diet + which glands are stimulated.
- Mucin
- Amylase (omnivores/horses NOT carnivores/ruminants)
- Bicarbonate (neutralisation/buffering)
- Phosphate (ruminants)
- Lysozyme/antibodies (reduce infection)
- Protein-binding tannins (leaf + bud eaters)
- Urea (ruminants

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2
Q

Salivary secretion in non-ruminants

A
  • primary secretion isotonic with blood
  • at low flow rates, secretion becomes hypotonic
  • at high flow rates secretion remains isotonic
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3
Q

Regulation of salivary secretion

A

Entirely under neural control
- Sympathetic - reduction in fight or flight
- Parasympathetic - increase during digestion

Basal salivary secretion for oral hygiene.

2 reflex pathways
- Congenital
- Conditioned

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4
Q

Congenital salivary reflex pathway

A

Initiated by taste/smell/presence of food in mouth
(in ruminants also by distension of orifices and rumination)

  • Afferent to salivary centre in brain
  • Efferent to salivary glands
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5
Q

Conditioned salivary reflex pathways

A

Pavlov dog experiments.
Initiated by repeated sensory stimuli associated with feeding
- Sight/smell of food
- Noise
Initiated in cerebral cortex and thence salivary centre in medulla oblongata

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6
Q

Motility

A
  • Segmental contractions - breakdown/mix
  • Peristaltic contractions
  • Anti-peristaltic contractions
  • Mass movement
  • Regulation of motility - chewing/initial swallowing/defaecation under voluntary control)
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7
Q

Chemical breakdown

A
  • Secretion of digestive juices
  • Salivary glands/liver/pancreas/glands in stomach + intestinal wall
  • Digestive juices extensively reabsorbed
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8
Q

Composition of digestive juices

A
  • Ions and pH appropriate for action of digestive enzymes
  • Mucus to lubricate food and protect mucosa
  • Enzymes to chemically breakdown food.
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9
Q

Enzymes involved in digestion

A

Carbohydrate:
- amylase, disaccharidases
(saliva/pancreas/intestinal mucosal surface)

Protein:
- pepsin/trypsin/peptidases
(stomach glands/pancreas/intestinal mucosal surface)

Fat:
- lipase, phospholipase
(pancreas/intestinal mucosal surface)

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10
Q

Absorption

A
  • Absorption is selective - most nutrients require specific transporter proteins
  • Active transport of nutrients
  • Directly by primary active transport
  • Indirectly by secondary active transport
  • Passive transport of nutrients
  • Facilitatively via transporter proteins
  • Diffusion down concentration gradient
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11
Q

Layers of the abdominal wall

A

Skin - can be tough in some species
- Variable cover in hair for insulation.

Subcutaneous fascia - superficial fascia
- Contains adipose (all over in pig, mainly inguinal area in others)
- Contains cutaneous trunk muscle (skin twitch)
Deep fascia (ox, horse)
- Developed into a tough fibro-elastic sheet = yellow abdominal tunic

Muscles

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12
Q

Muscles of the abdominal wall

A

4 muscles
Lateral (outside to inside):
- External abdominal oblique m.
- Internal abdominal oblique m.
- Transverse abdominal m.
Ventrally:
- Rectus abdominis

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13
Q

Functions of abdominal wall muscles

A

Encloses the abdominal cavity and its contents.
Motor functions:
- Contraction causes increase in intra-abdominal pressure
(used in vomiting, defaecation and micturition)
- If larynx is closed, also causes increase in intra-thoracic pressure (via diaphragm)
(used in breathing, coughing, sneezing)

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14
Q

Rectus abdominis m.

A
  • Straight abdominal muscle
  • 6 pack in humans
  • Originates on ventral surface of sternum/sternabrae
  • Inserts on cranial border of pubis via pre-pubic tendon
  • Left and right sides separated by linea alba
  • in immature animal, linea alba is pierced by umbilicus
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15
Q

External oblique abdominal m.

A
  • Outermost lateral abdominal wall muscle
  • Originates on lateral caudal surfaces of rubs 4+ and lumbodorsal fascia
  • Inserts on linea alba and prepubic tendon
  • Fibres run obliquely from cranio-dorsal to caudo-ventral
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16
Q

Internal oblique abdominal m.

A
  • Middle lateral abdominal wall muscle
  • Original on coral tuber and lumbodorsal fascia
  • Inserts on linea alba, last rib & cartilages of caudal ribs
  • Fibres run obliquely from caudo-dorsal to cranio-ventral
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17
Q

Transverse abdominal m.

A
  • Innermost lateral abdominal wall muscle
  • Originates on medial surfaces of ventral parts of caudal ribs and deep lumbodorsal fascia
  • Inserts on linea alba
  • Fibres run transversely
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18
Q

Sheath of Rectus Abdominis m.

A
  • Foremed from the tendons of the lateral abdominal wall muscles
  • They pass above/below rectus abdominis m. to join in the midline
  • This join is to referred to as “aponeurosis” and forms the linea alba
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19
Q

Innervation

A
  • Innervation by spinal nerves of last thoracic vertebra & L1-L5
  • Dorsal roots innervate dorsal musculature
  • Ventral roots split into 3 branches
    Medial - runs between TA + IAO down to RA
    Lateral - runs IAO + EAO down to midway
    Lateral cutaneous - perforates EAO to innervate skin
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20
Q

Inguinal canal

A
  • Internal oblique muscle has gap (=deep inguinal ring)
  • External oblique muscle has slit (=superficial inguinal ring)
  • Inguinal canal = potential space between these 2 slits
  • Significance of this will be covered in urogenital fortnight
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21
Q

Embryology of GI tract

A
  • Epithelium lining GI tract & associated exocrine gland = endoderm
  • Muscle & connective tissue = splanchnic mesoderm
  • As embryo develops part of yolk sac taken into body
    • This goes on to form the gut
    • Midgut separated from foregut/hindgut by cranial intestinal portals
    • Foregut/hindgut end blindly at oral/cloacal plates
  • Foregut differentiates into pharynx, oesophagus, stomach nd initial duodenum
  • Midgut differentiates into rest of duodenum, jejunum, ileum, caecum, ascending/transverse colon
  • Hindgut differentiates into descending colon and rectum
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22
Q

Peritoneum

A
  • Serous membrane that lines abdominal cavity & envelops abdominal organs
  • SIngle continuous sheet
    • Parietal peritoneum
      • Closely adherent to abdominal wall
      • Extends through inguinal canal
    • Visceral peritoneum
      • Closely adherent to abdominal canal
      • Envelops organs
    • Connecting peritoneum
      • Mesentary - connects bowel to body wall
      • Omentum - connects stomach to something
      • Fold - connects bowel to bowel
      • ligament - connects non-bowel to something
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23
Q

Topographical anatomy

A

The relationship of organs within the abdomen

Defined by the peritoneal attachments - to one-another or body wall

Aids or hinders surgical access - the peritoneum

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24
Q

Cavities

A

Abdominal cavity
- Defined by diaphragm cranially
- Abdominal wall laterally
- Contains all abdominal organs/structures including peritoneum

Peritoneal cavity
- The potential space between parietal & visceral peritoneum
- Contains nothing other than a small amount of peritoneal fluid - unless peritoneal inflammation = peritonitis

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25
Q

Diaphragm

A
  • Separates thorax from abdomen
  • Attaches to body wall at level of last rib
  • Extends into thorax to level of 5th inter-costal space
  • Aorta passes through aortic hiatus between left + right crura
  • Caudal vena cava passes through caval foramen in central tendon
  • Oesophagus passes through oesophagus hiatus
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26
Q

Connecting peritoneum

A

Mesentary - connects bowel to body wall

Omentum - connects stomach to something

Fold - connects bowel to bowel

Ligament - connects non-bowel to something

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27
Q

Liver

A

4 lobes
- L&R lobes (split into medial and lateral in dogs)
- Caudate
- Caudate process
- Papillary process
- Quadrate

Peritoneal attachments:
- Coronary ligament
- R&L triangular ligaments
- Falciform/round ligament

Gallbladder
- Cystic/hepatic/common bile ducts

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28
Q

Stomach

A

3 areas:
- Fundus = blind ending
- Corpus = body
- Pylorus (pyloric antrum)

Peritoneal attachments:
- Greater omentum
- Lesser omentum - hepato-gastric ligament
- Gastro-splenic ligament

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29
Q

Spleen

A
  • On LHS of abdomen
  • Blood reservoir
  • Abnormally enlarged in barbiturate euthanasia

Peritoneal attachments:
- Gastro-splenic ligament

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30
Q

Duodenum

A
  • First part of small intestine
  • Exit of bile duct/pancreatic duct on major duodenal papilla
  • Exit of accessory duct on minor duodenal papilla

Peritoneal attachments
- Mesoduodenum
- Duodeno-colic fold
- Hepato-duodenal ligament (part of lesser omentum)

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31
Q

Jejunum

A
  • Middle part of small intestine
  • Largest proportion of SI
  • Covered by greater omentum

Peritoneal attachements:
- Meso-jejunum/mesentary (fan shaped)

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32
Q

Ileum

A
  • Terminal portion of SI
  • Enters into LI at caeco-colic junction

Peritoneal attachments:
- Ileo-caecal fold
- Meso-ileum (extension of meso-jejunum)

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33
Q

Pancreas

A

2 lobes:
- Right lobe running in cranio-caudal direction
- Left lobe running media-laterally

Peritoneal attachments:
- Right lobe within meso-duodenum
- Left lobe within deep leaf of greater omentum

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34
Q

Caecum

A
  • First part of LI
  • Blind ending sac
  • In dog, ileum runs directly into colon, with caecum attached on side
  • In other species, caecum is continuous with colon and ileum enters LI at caeca-colic junction
  • NOT the appendix

Peritoneal attachments:
- Ileo-caecal fold
- Caeca-colic fold

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35
Q

Colon

A

Ascending (right):
- Right colic flexure
- Transverse - passes cranial to root of mesentery
Descending (left):
- Left colic flexure
- Rectum

Peritoneal attachments:
- Meso-colon to dorsal body wall

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36
Q

Enteric nervous system

A
  • Short reflex arcs located within wall of GI tract
  • Can operate independently of rest of body
  • 2 nerve plexuses that synapse with each other.
    • Sensory cells respond to:
      • Content of lumen
      • Degree of wall stretch
    • Motor cells stimulate
      • Smooth muscle cells (motility)
      • Epithelial cells (digestive juices/hormones)
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37
Q

Enteric nervous system 2

A
  • Simple reflex arc; consists of a single motor neurone
  • Complex reflex arcs consist of simple reflex arcs connected by interneurons - nerve impulse is propagated wider.
  • Short reflex arcs enable GI tract to have extensive control of its activities
  • Most reflexes are stimulatory and cholinergic
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38
Q

Autonomic nervous system

A

Parasympathetic promotes digestion
- Pre-ganglionic fibres run in vagus (cholinergic)
- Post-ganglionic fibres embedded in wall of GI tract and connect to ENS (cholinergic)

Sympathetic inhibits digestion
- Pre-ganglionic fibres run in splanchic nerves (cholinergic)
- Post-ganglionic fibres run along arteries to organ of innervation or in hypogastric nerves
- Synapse with ENS to reduce Ach release at parasympathetic pre-synapses
- Adrenergic to inhibit secretion + motility and decrease perfusion to GI tract

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39
Q

Autonomic Nervous System 2

A
  • Connection to CNS (sight/smell/taste)
  • Entero-enteric reflexes - coordinate activity between different parts of GI tract
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40
Q

Phases of regulation

A

Cephalic phase:
- Anticipation of food (Pavlov’s)
- Emotion
- Coordinated by ANS

Gastric phase:
- Stomach distension/presence of peptides
- Coordinated by ANS, ENS and hormones (mainly gastrin)

Intestinal phase:
- Intestinal distension/lumen contents
- Coordinated by ANS, ENS and hormones

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41
Q

Regulation of Appetite

A
  • Controlled by hypothalamus
  • Appetite centre (ventro-lateral hypothalamus) - has direct effect on animal’s behaviour
  • Satiety centre (ventro-medial hypothalamus) - causes refusal of food, inhibits appetite centre

3 theories for mechanism of action:
- Glucostat theory - regulated by levels of glucose
- CCK theory - regulated by levels of CCK
- Lipostat theory - regulated by levels of fat

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42
Q

Motility

A

Coordinated contraction of smooth muscle in GI tract

1) Segmental
- Mixes lumen contents/breakdown (stomach)

2) Peristalsis
- Moves intestinal contents in gradual aboral direction

3) Anti-peristalsis
- Moves intestinal contents in oral digestion

4) Mass movement
- Empties entire sections of GI tract

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43
Q

Pacemaker cells

A

Repetetive + spontaneous oscillations (~5/min) in membrane potential occur in groups of pacemaker cells (interstitial cells of Cajal)
- Located between circular + longitudinal smooth muscle
- Synchronisation of smooth muscle contractions achieved by transfer of oscillations to smooth muscle via gap junctions

  • If stimulus absent, depolarisation is too weak to reach threshold potential = no muscle contraction
  • If stimulus present, depolarisation reaches threshold potential = action potential to cause smooth muscle contraction
  • Action potential due to opening of Ca2+ channels
  • Frequency of action potentials determines strength of contraction.
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44
Q

Swallowing/deglutition

A
  • Propulsion of food from oral cavity into oesophagus
  • Food mould into bolus by tongue and moved upwards and backwards to pharynx
    • under voluntary control
    • forces soft palette up to seal off nasal cavity
  • Pressure-sensitive sensory cells stimulated
    • swallowing centre in medulla initiates swallowing reflex
    • under involuntary control
  • Epiglottis closes off trachea
  • Complicated contraction/relaxation of muscles force food into oesophagus
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45
Q

Swallowing disorders

A
  • Failure of soft palette to close off nasal cavity
  • Failure of epiglottis to close off trachea
  • Pharangeal paralysis
    • nerve/muscle injury
  • Botulism - clostridial toxins block Ach release
  • Myaestheania gravis
    • antibodies formed against Ach receptors
  • Anaestesia
    • may anapestics induce vomiting
    • swallowing process impaired
    • inhalational pneumonia
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46
Q

Anatomy of the oesophagus

A

Mucosal layer
- Stratified squamous epithelium

Submucosal layer
Muscular layer
- Inner circular/outer longitudinal
- Composed of striated + smooth muscle

Serial layer
- Adventitia (loose connective tissue) only in neck - slower healing in surgery

True serial layer in thorax

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47
Q

Innervation of the oesophagus

A

Sympathetic - via cervical sympathetic chain

Parasympathetic
- SVE/AA via recurrent laryngeal (cranial division of XI) to cranial cervical oesophagus
- AE/AA via vagus to caudal cervical/thoracic oesophagus
- species with striated muscle in caudal oesophagus still innervated by parasympathetic

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48
Q

Transport down oesophagus

A

Upper oesophageal sphincter closes behind food bolus (epiglottis opens to allow breathing)

complicated peristaltic contractions force food down oesophagus - animals can swallow upwards

Lower oesophageal sphincter opens to allow passage of food into stomach

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49
Q

Lower oesophageal sphincter

A

= Cardiac sphincter
Physiological rather than anatomical - except in horses

always closed except during swallowing

oesophagus enters abdomen at oblique angle
- Higher pressure in abdomen cf thorax causes stomach to exert pressure on diaphragm; reinforcing closure

prevents regurgitation of acidic stomach contents

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50
Q

Vomiting/emesis

A

Active propulsion of stomach contents into oral cavity.
- Deep inspiration with simultaneous closure of trachea/nasal cavity
- increases intra-abdominal pressure via diaphragm

Forceful contraction of abdominal muscles - NOT gastric muscles

Cardiac sphincter opens

Food propelled up oesophagus

Upper oesophageal sphincter opens

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51
Q

Vomiting/emesis 2

A
  • Controlled by vomiting centre in medulla
  • Stimulated by pharyngeal/gastric distension/irritation
  • Normal in dogs/cats to expel bones/hair
  • Ruminants prefer to regurgitate

Horses/rats
- Very well developed cardiac sphincter
- Exaggerated oblique entry through diaphragm
- Stomach usually ruptures before vomiting occurs

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52
Q

Gastric torsion

A
  • Occurs in horses and wide-chested dogs
  • Stomach rotates 90-360°
  • Seals off cardiac sphincter; preventing vomiting
  • Stomach distends further with gas
  • If rotation compromises blood supply, gastric tissue becomes oedematous/hypoxic and necrotic
  • Stomach dilation can impair venous return to heart via caudal vena cava resulting in circulatory shock
  • Extreme emergency requires surgical intervention
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53
Q

Functional anatomy of simple stomach

A

Functions:
- Digestion
- Continuation of starch digestion
- Initiation of protein digestion

  • Protection
    • Stomach acid kills bacteria ingested with food
  • Storage
    • Ensures food delivered to SI at controlled rate
  • Mechanical breakdown/mix
    • Breaks food + mixes with gastric juice to form a semi-liquid chyme

Abomasum is ruminant equivalent of simple stomach

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54
Q

Embryological regions of the stomach

A

Oesophageal region:
- Non-glandular
- Stratified squamous
epithelium

Cardiac region:
- Secretes mucous only

Fundic region:
- Secretes mucous/gastric juice

Pyloric region:
- Secretes mucous only
- Regulates stomach emptying

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55
Q

Anatomical regions of the stomach

A

Cardia - entrance to stomach
- Physiological valve

Fundus - blind ending part of stomach

Corpus - body of stomach

Pylorus - exit from stomach

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56
Q

Cell types in stomach

A

Consist of cylindrical glands

Mucous/goblet cells
- Secrete mucous to protect against HCl

Parietal/oxyntic cells
- Secrete HCl to digest protein

Chief/peptic cells
- Secrete pepsinogen to digest protein

Entero-endocrine cells
- Secrete hormones

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57
Q

Motility of the stomach

A

Serves to:
- Prepare stomach to receive a meal
- Mix and mechanically break down chyme
- Empty stomach contents to SI
- Prevent regurgitation of stomach contents into oesophagus

When an animal starts eating there is an initial relaxation of stomach smooth muscle to accommodate the meal - receptive relaxation
- Regulated by swallowing centre via vagus
- Transmitter = vasoactive intestinal peptide - NOT Ach

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58
Q

Motility of the stomach 2

A
  • Mainly peristalsis
  • Start in fundus with weak contractions
  • Propagate down corpus
  • Pyloric sphincter opens to allow chyme into duodenum
  • When contractions reach pylorus, pyloric sphincter closes
  • Food forced back into corpus helps mixing
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59
Q

Regulation of stomach emptying

A
  • Mainly regulated by strength of contraction
  • Also opening/closing of pyloric sphincter
  • Stimulation of emptying
    • Neural regulation - expansion of stomach walls increases strength of contraction
    • Hormonal regulation - release of gastrin increases strength of contraction and dilates pyloric sphincter
  • Inhibition of emptying
    • Factors in duodenum act to inhibit gastric contractions
      • increased pressure in walls
      • Low pH
      • High [fat/peptide]
      • High osmolarity
      • Neural regulation via increased sympathetic activity/decreased parasympathetic activity via vagus
      • Hormonal regulation via secretin, cholecystokinin & gastric inhibitory peptide (GIP)
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60
Q

Digestion in simple stomach

A

Enzymatic breakdown of nutrient macromolecules into smaller units that can be absorbed

Starch
- Digested by amylase
- Only active at pH > 6
Protein
- Digested by pepsin
- Only active at low pH

How can both of these enzymes function in the stomach?

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61
Q

Structure of starch

A
  • Complex carbohydrate
  • A mixture of amylose and amylopectin
  • Basic unit is maltose
  • Amylose comprises double helix of maltose units linked by 1-4 ⍺-glycosidic bonds
  • Amylopectin comprises of branching chain of maltose units linked by 1-6 ⍺-glycosidic bonds

Amylase can digest ⍺-glycosidic bonds but not β-glycosidic bonds found in cellulose

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62
Q

Starch digestion

A
  • Initiated by salivary amylase in mouth
  • BUT food doesn’t spend much time in mouth before it is swallowed
  • Newly swallowed food forced into centre of stomach
  • Acid secreted from stomach walls
  • Gradual decline in pH from centre of stomach to edge that allows starch digestion to continue
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63
Q

Comparative starch digestion

A

Omnivorous diets contain high levels of starch
- Pigs have adapted stomachs to allow starch digestion to continue longer

Herbivorous diets contain low levels of starch
- Working horse diets have increased levels of starch
- Horses have adapted their stomachs to allow starch digestion to continue longer

Carnivorous diets contain low levels of starch
- Carnivore saliva doesn’t contain amylase (digest starch in SI)

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64
Q

Comparative salivary amylase levels

A
  • High in pigs
  • Low in horses as diet usually contains low levels of starch
  • Absent in carnivores + ruminants
  • Very high in humans as stomach not adapted for starch digestion
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65
Q

Protein digestion

A

Gastric juice consists mainly of HCl + pepsinogen
- Pepsin is inactive until it comes into contact with foreign protein as organs are made of protein

Pepsinogen must be converted into pepsin before it can digest protein

Stomach mucosa very resistant to digestion
- Breach of mucosal barrier -ulceration

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66
Q

Functions of HCl

A

Convert inactive pepsinogen into its active form - pepsin

Provides the required acidic environment for pepsin to digest protein

Prevents fermentation by killing microbes
- In pigs/horses some fermentation of starch into VFAs occurs as large part of stomach doesn’t produce acid

Degrades large chunks of connective + muscle tissue into smaller, more digestible parts

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67
Q

Secretion of HCl

A

Duration and volume depends on species
- Max secretion occurs 2-3 hours after a meal in dogs cf pigs (almost continuous)

HCl secreted by parietal/oxyntic cells

Stomach pH reaches 2.0-2.5

Opposite process occurs in pancreas to neutralise pH of food passing into duodenum

Urine pH increases just after a meal due to delay between food passing from stomach to pancreas

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68
Q

Secretion of pepsinogen

A

Synthesised + stored in chief/peptic cells

Pepsinogen secreted in inactive form

Activated by HCl in stomach

Pepsin initiates degradation of protein and collagen by breaking peptide links adjacent to aromatic amino acids
- These peptides stimulate further HCl secretion

Pepsin can activate more pepsinogen - auto-catalysis

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69
Q

Stimulation of secretion

A

Reflex arcs
- Long via vagus
- Short locally

3 substances
- Amplify eachother
- Ach/histamine
- Direct stimulation
- Chief (pepsinogen. parietal (HCl) & mucin cells

Gastrin
- Almost entirely via stimulation of ECL cells to produce histamine
- Mainly parietal cells (HCl)

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70
Q

Cephalic phase

A

Neural stimulation:
- Before food has entered stomach
- Caused by sight, smell, taste
- Stimulates secretion
- Directly via Ach
- Indirectly via gastrin in blood

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71
Q

Gastric phase

A

Neural stimulation:
- After food has entered stomach
- Caused by
- Stomach expansion
- Peptides in lumen
- Stimulate secretion
- Directly via Ach
- Indirectly via gastrin in blood

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72
Q

Intestinal Phase

A

After food has entered duodenum

Stimulation or inhibition
- Depends on acidity of chyme
- Food components

Stimulation via neural (cholinergic) + hormonal signals
- CCK role varies according to species
- Dogs = partial agonist (low H+) or strong antagonist (high H+) cats = strong agonist

Most intestinal responses = inhibitory

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73
Q

Hormonal stimulation

A
  • Mediated by gastrin
  • Mainly in response to peptides in stomach
  • Reaches target cells via blood
  • Maximal HCl secretion requires simultaneous by Ach, histamine and gastrin
  • Gastrin mediates its effect almost entirely via stimulation of ECL-cells to release histamine
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74
Q

Inhibition of secretion

A

Duodenal signals that inhibit stomach motility also inhibit gastric juice secretion
- Hormonal via vagus
- Hormonal
Localised inhibition in stomach too
- pH<2.0 stops gastrin release to protect gastric mucosa from damage
- Before food enters stomach, H+ low but not buffered so gastrin inhibited
- Once food enters stomach with buffers (mainly protein) H+ reduced so gastrin released again
- More protein in diet –> more gastrin release

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75
Q

Gastric/duodenal ulceration

A

Stomach mucosa protected from HCl by:
- Secretion of mucous layer
- Epithelial CM and interconnecting tight junctions impermeable by H+
- Epithelial cells replaced every 2-3 days

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76
Q

Ulceration pathophysiology

A

Increased acid production (duodenal ulcers)

Decreased protective functions (gastric ulcers)

HCl + pepsin damage epithelial cells and underlying tissues = ulceration

Damaged cells produce histamine which stimulates acid secretion and intensifies problem

Diarrhoea due to increased secretion + decreased absorption (villi damaged by acid)

Faeces appear dark red/black

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77
Q

Ulceration Aetology

A
  • H Pylori in humans
  • NSAIDs
    • inhibit prostaglandin synthesis (prostaglandins stimulate production of mucous and bicarbonate)
    • Protective mechanisms reduced
  • Mast cell tumours/leukaemia
    • Produce XS histamine
    • Increases HCl production
  • Gastrin-producing tumours
    • Produce XS gastrin
    • Increases HCl production
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78
Q

Ulcer treatment

A

Aimed at reducing HCl secretion
- Anti-histamines
- Proton Pump Inhibitors

Protecting ulcerated mucosa
- Antacids
- Mucosal Binding Agents

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79
Q

Digestion + Absorption (intestines)

A

SI is major site of digestion + absorption in simple stomached mammals

Absorption is selective process occurring via specific transporter proteins by
- Diffusion down conc gradient
- Secondary active transport

Most organic nutrients + monovalent ions absorbed irrespective of body requirements

Divalent ions + trace elements absorbed depending on body requirements

SI has large reserve capacity
- Up to 50% can be resected without hindering digestion/absorption

Most nutrients absorbed along entire length of SI

2 phases of digestion
- Luminal - enzymes secreted by salivary glands/pancreas
- Membranous - enzymes attached to epithelial surface of intestinal cells

Anything remaining undigested by SI passes on to LI for microbial fermentation

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80
Q

Functional anatomy of SI

A

3 parts
- Duodenum - 15% of length
- Jejunum - 75% of length
- Ileum - 10% of length

Standard intestinal structure
- Mucosa
- Submucosa
- Muscle (inner circular/outer longitudinal)
- Serosa

Surface area massively increased for absorption by:
- Mucosal folds
- Villi
- Microvilli

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81
Q

Cell types (intestine)

A

4 types of intestinal epithelial cell
- Goblet cells secrete mucous for lubrication + protection of mucosa and bicarbonate for neutralisation of stomach acid
- Enteroendocrine cells control digestive function via sensory mechanisms and release of hormones
- Paneth cells possibly involved in defence against microbial penetration
- Enterocytes (majority of cells) responsible for absorption via transporter proteins
- contain many brush border digestive enzymes
- enzymes remain attached to epithelial membrane

Continuous turnover of cells with migration from crypts up villus
- Sloughed off at villus tip
- Migration takes 2-5 days

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82
Q

Motility of SI

A

Serves to:
- Mix luminal contents
- Segmental contractions (digestive period)

  • Propel contents down SI at appropriate rate to allow max digestion + absorption
    • Peristaltic contractions (inter-digestive period)

SI emptying
- Circular muscle at ileo-caecal junction well developed
- Functions as physiological valve/sphincter
- Especially pronounced at ileo-caecal junction in horses
- Motility of stomach increases after feeding
- Ileal contractions increase
- Ileo-colic sphincter relaxes
- Facilitates emptying of SI to colon
- Gastro-ileal reflex

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83
Q

Segmental contractions

A

CIrcular contractions occur along distended intestine
- Divide intestinal contents into small segments
- New contractions occur in centre of distended segment
- Repeated many times
- Mixes contents with digestive juices
- Moves contents towards mucosal surface for digestion/absorption

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84
Q

Segmental contractions 2

A

Main type of contraction during digestive period
- Intense contractions upon emptying of stomach

  • Short periods of weak segmental contractions
    • allows weak peristaltic contractions to occur
    • BUT they soon die out
    • Overall a slow aboral movement of chyme occurs
  • As chyme reaches distal SI, feedback mechanism inhibits proximal contractions
    • Mediated via neural/hormonal mechanisms
    • major mechanism for coordinating SI transit to allow maximal digestion/absorption
    • SI transit ~3-4 hours in most species regardless of size
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85
Q

Peristaltic contractions

A

Main type of contraction when digestion/absorption complete (inter-digestive period)
- Irregular moderate peristaltic activity
- Propagates a short distance
- Regular strong peristaltic activity
- Propagates a long distance

  • Each new contraction starts slightly further down the SI
  • When a peristaltic contraction reaches ileum, a new one starts in duodenum
    • Migrating Myo-electric complex
    • Takes ~1-2 hours to propagate down entire SI
    • Empty SI of contents
    • Prevent retrograde flow from colon
  • Peristalsis can occur in reverse but reverse contractions die out quickly in SI
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86
Q

Propagation of peristalsis

A

Most motor neurone of ENS release Ach
- Stimulates smooth muscle contraction

Some inhibitory transmitters released too

Distension of segment causes stimulation + inhibition
- Longitudinal muscle relaxes/circular muscle contracts behind chyme
- Longitudinal muscle contracts/circular muscle relaxes in front of chyme

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87
Q

Regulation of motility (intestine)

A

Controlled by interstitial cells of Cajal = pacemaker cells

Spontaneous oscillations always present
- Independent of neuronal/hormonal influences
- Highest frequency of slow waves in duodenum declining towards ileum
- Duodenum can inhibit stomach emptying if chyme causes too much distension
- If sufficiently depolarised, multiple action potential spikes occur, causing smooth muscle contraction
- Propagate from cell-cell via gap junctions
- Strength of contraction determined by number of action potential spikes occurring

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88
Q

Regulation of motility (intestines) 2

A

Mainly regulated by ENS

Presence of chyme in duodenum stimulates short reflex arcs dependent on degree of distension

Strength of contraction increased by parasympathetic/decreased by sympathetic control
- Major function of ANS is to coordinate motility in different parts of the GI tract via long reflex arcs

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89
Q

Carbohydrate digestion + absorption (intestines)

A

Provide most of energy in herbivores/omnivores
- Polysaccharides
- ⍺-glycosidic bonds - digestible by mammalian enzymes
- β-glycosidic bonds - requires microbial fermentation

  • Disaccharides
    • Maltose
    • Sucrose
    • Lactose
  • Monosaccharides
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90
Q

Carbohydrate digestion

A

Only monosaccharides can be absorbed

  • Luminal digestive phase:
    • Starch/amylose –> maltose
    • Salivary amylase continues digestion in SI with pancreatic amylase
  • Membranous digestive phase
    • Maltose –> glucose x2
    • Sucrose –> glucose + fructose
    • Lactose –> glucose + galactose
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91
Q

Disaccharidases

A

Disaccharidases attached to enterocyte brush border

  • Maltase/Sucrase/Lactase
  • Digestion of maltose/sucrose very quick - rate of absorption is limiting factor
  • Lactose digestion is much slower - absorption rate is limiting factor
  • Disaccharidase levels change with age
    • Neonate - high lactase/low maltase
    • Adult - low lactase/high maltase
    • Ruminants - no sucrase
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92
Q

Carbohydrate absorption

A

Glucose and galactose absorbed by sodium glucose co-transporter (SGLT1)
- Secondary active transport
- Na+ & glucose bind to transporter on luminal side
- Conformational change in transporter moves Na+ & glucose/galactose into cell and release them into cytosol
- High levels of Na+ in digestive juice maintain luminal concentration of Na+ high
- Concentration of glucose/galactose in cytosol high so diffuse down gradient into blood via facilitative transporter GLU2

Fructose absorbed down concentration gradient by facilitative transporter (GLUT5)
- Passive transport
- Diffuse out of cytosol down concentration gradient into blood via GLUT2

Transferred to liver via hepatic portal vein

Stored as glycogen or continue in circulation to be metabolised for energy

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93
Q

Secondary active transport

A

Na+ moves from lumen into enterocyte down its concentration gradient

Energy from this used to co-transport glucose/galactose

Na+ gradient maintained by Na+/K+ ATPase on basolateral membrane

Moves 3 Na+ ions out of cell in exchange for 2 K+ ions
- Maintains net -ve charge in cell

Requires ATP (primary active transport)

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94
Q

Adaptation to diet (intestines)

A

Some digestive/absorptive functions regulated by diet

Others are pre-programmed to appear at a certain phase of life and then disappear irrespective of diet

Omnivores:
- Diet contains high levels of bicarbonate
- SGLT1 levels remain high
- Expressed high throughout SI

Ruminants
- SGLT1 expression in lambs is high
- As rumen develops, less bicarbonate passes into SI
- SGLT1 expression declines to negligible amounts in adult grazers
- Maintained in intermediates/browsers as some bicarbonate bypasses fermentation and passes into SI

Horses
- SGLT1 highest proximally declining distally in wild horses on grass
- To compete, domestic horses fed increased levels of bicarbonate
- Consequently SI adapts by increasing levels of SGLT1 overall but especially proximally

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95
Q

Lactose intolerance

A

Main carbohydrate in milk is lactose

Requires lactase to digest

Lactase activity high in neonate but programmed to decline as animal is weaned
- Lactase levels low/negligible in adults
- EXCEPT caucasians

In absence of lactase, lactose accumulates in gut lumen
- Osmotic force -> decreased water absorption (diarrhoea)
- Once reaches LI fermented
- Lactic acid cause pH to decline upsetting microbial balance
- Lactate poorly absorbed cf VFAs - creates osmotic effect to further decrease water absorption
- Gas products cause distention in pain/discomfort

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96
Q

Protein digestion + absorption

A

Carnivorous/omnivorous diets high in protein

Herbivorous diets low in protein - BUT ruminant SI receives lots of protein in the form of microbial protein passing from rumen

Protein digestion initiated in the stomach

Continues in SI with pancreatic proteases (luminal phase of digestion)

End products of digestion are di/tri-peptides and amino acids
- Most protein absorbed as di/tri-peptides
- Amino acids transported into enterocytes via Na+ co-transport similar to monosaccharides (secondary active transport)
- Di/tri-peptides transported into enterocytes via H+ co-transport

Transported out of enterocyte down their concentration gradient via facilitative transporters

Enzymatic digestion very fast therefore rate limiting step is absorption.

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97
Q

Protein digestion in neonates

A

Proteins can’t be absorbed as they would be regarded as foreign material and evoke an immune reaction

In neonates, the immune system is poorly developed

Placental transfer of maternal antibodies occurs via colostrum in the 1st 24-36 hours of life

To enable absorption of intact protein
- Epithelial cells of intestine are permeable to intact protein
- Stomach products negligible amounts of HCl
- Pancreatic enzyme secretion is low
- Colostrum contains trypsin inhibitors

Consequently large amount of maternal antibody can absorbed in the 1st 24 hours to provide passive immunity to the neonate

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98
Q

Functional anatomy of the pancreas

A

Microscopic structure of exocrine pancreas similar to salivary gland
- Groups of acini
- Simple cuboidal epithelium surrounding an excretory duct
- Several excretory ducts combine with increasing dimension to terminate as pancreatic duct/accessory pancreatic duct

Microscopic structure of endocrine pancreas consists of lots of isolated clumps of cells surrounding a capillary (islets of Langerhans)

2 major functions
- digestion (exocrine pancreas)
- regulation of metabolism (endocrine pancreas)

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99
Q

Exocrine pancreas

A

Principal function is digestion

Pancreatic juice has 2 major components
- bicarbonate to neutralise stomach acid thereby protecting SI mucosa
- also provide the correct pH for digestive enzymes
- Enzymes to digest food material for absorption in SI
- Involved in carbohydrate/protein/fat digestion

In horse/pig substantial amounts of pancreatic juice produced to create a large intestinal environment suitable for fermentation
- Equivalent to saliva production in ruminants

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100
Q

Ionic composition of pancreatic juice

A

Similar to blood.

HCO3- actively transported into duct lumen in exchange for chloride
- Water follows by osmosis
- H+ transported into bloodstream
- negates alkaline tide
- At normal flow rates, HCO3- reabsorbed into acing cells
- At high flow rates (during digestion) not enough time for reabsorption so pancreatic juice remains highly alkaline
- Na+/K+ composition constant whatever the flow rate

101
Q

Enzymatic composition of pancreatic juice

A

Secretion of digestive enzymes for carbohydrate/fat/protein breakdown
- Proteases secreted in inactive form to prevent auto-digestion
- Amylase breaks down starch (continues where salivary amylase left off)
- Lipases/phospholipases breakdown fat to glycerol/fatty acids

102
Q

Activation of enzymes

A

Pancreatic juice contains trypsinogen/inactive proteases

Duodenal epithelial surface contains enteropeptidase
- Trypsinogen –> trypsin

Trypsin auto-catalyses itself as well as activating other proteases

As a precaution, pancreatic cells produce trypsin inhibitor to prevent auto-digestion

103
Q

Regulation of secretion (pancreas)

A

3 phases to digestion
- Cephalic phase
- Gastric phase
- Intestinal phase

All phases increase pancreatic juice secretion

Cephalic/gastric mediated by vagus/gastrin
- Carnivores - only enzymatic component
- Horse/pig - ionic component as well (for LI fermentation)

Intestinal phase mediated by secretin/CCK
- Causes largest increase in secretion
- Vasoactive inhibitory peptide inhibits effect of secretin

104
Q

Secretin

A
  • Released from duodenum in response to H+
  • Increases HCO3- secretion
  • Negative feedback mechanism
    • As acid chyme gradually neutralised stimulus for secretin release diminishes
105
Q

Cholecystokinin (CCK)

A

Released from duodenum in response to fat/protein metabolites

Increases enzyme secretion

Also causes gall bladder to contract

Positive feedback mechanism
- Increased enzyme secretion produce more metabolites which in turn stimulate further CCK release

106
Q

Comparative physiology (pancreas)

A

Differences due to pattern of eating

Ruminants
- Continuous flow of rumen contents into abomasum/SI - pancreatic juice secretion continuous irrespective of eating

Carnivores/omnivores
- Intermittent flow of stomach contents into SI - pancreatic juice secretion intermittent

Horses
- Continuous flow of stomach contents into SI - pancreatic juice secretion continuous
- BUT also increases after feeding cf ruminants
- Horse pancreatic juice low in HCO3-
- able to neutralise acidic stomach components due to copious secretion of HCO3- by ileum

107
Q

Endocrine pancreas

A

Principle function is regulated of metabolism

Clusters of cells scattered throughout the pancreatic tissue = islets of Langerhans
- 1-2% of pancreatic mass
- 3 major types of cell β~65% ⍺~25% δ~10%

Hormones
- Insulin - produced by β-cells
- Glucagon - produced by ⍺-cells
- Somatostatin - produced by δ-cells - paracrine effect to inhibit both insulin + glucagon secretion

Secreted in bloodstream and passes to liver via hepatic portal vein prior to circulating to other tissues

108
Q

Insulin

A

Peptide hormone released in response to increased plasma levels of glucose + amino acids

Overall anabolic effect

Produced in pancreatic β-cells
- Synthesised as pre-pro-hormone
- Converted to pro-insulin
- Inactive due to c-peptide
- Secreted as active insulin by cleavage of the C-peptide
- Plasma half life of 5-8 mins
- Deactivated in liver by cleavage of di-sulphide bonds

109
Q

Regulation of insulin

A

Stimulated by increase in plasma glucose

Also by increase in plasma amino acids

Direct feedback mechanism independent of other factors

Bi-phasic secretion
- Initial immediate secretion of stored insulin lasting 5-15 mins
- Followed by more prolonged secretion of newly synthesised insulin adjusted to plasma levels of glucose

Also stimulated by GI hormones released when food enters duodenum

Thus insulin secreted in anticipation of increased absorption of glucose/amino acids
- Insulin secretion greater when glucose administered orally cf intra-venously

110
Q

ANS regulation of insulin

A

Parasympathetic activity via vagus increases insulin secretion
- Part of long-reflex arc
- Amplifies hormonally-regulated secretion

Sympathetic activity + adrenaline releases decreases insulin secretion

111
Q

Actions of insulin

A

Binds to receptors on target cells
- Receptor functions as a tyrosine kinase upon activation
- Phosphorylation of intra-cellular proteins mediates different actions of insulin

Stimulates cell uptake of nutrients during absorptive phase

Most important anabolic mediator

Glucose uptake enhanced by mobilisation of glucose transporter (GLUT4) to cell membranes
- Nearly all tissues (esp skeletal muscle/adipose tissue)
- Brain, liver, intestines, kidney + mammary tissue insulin-independent
- Glucose uptake mediated by different GLUT transporters

112
Q

Actions of insulin 2

A

Amino acid uptake enhanced by amino-acid transporter proteins
- Nearly all tissues
- Increases intra-cellular amino acids for energy + protein synthesis (anabolic effect)

Increases concentration/activity of intra-cellular enzymes involved in metabolism of glucose/amino acids/lipids
- Especially in liver, skeletal muscle, adipose tissue
- Increases glycogenesis in liver/FFA for tri-glyceride synthesis
- Inhibits enzymes that breakdown try-glycerides

113
Q

Diabetes Mellitus

A

Plasma glucose elevated (hyperglycaemia) due to decreased uptake by cells

Capacity for kidneys to re-absorb glucose exceeded (glycosuria)

Fairly rare but occurs most often in carnivores/omnivores

2 types
- Type I - insulin-dependent
- Insulin production impaired
- Treated by insulin injections
- Type II - non-insulin dependent
- Cells resistant to insulins effects

IDDM most common
- Caused by pancreatic inflammation, hyper-secretion of hormones antagonistic to insulin

114
Q

Diabetes 2

A

Hyperglycaemia - polydipsia/polyuria
- Would expect urine specific gravity to be low but artificially normal/high due to glucosuria
Degradation of lipids increases leading to increased plasma FFA
- Incomplete metabolism of FFAs results in production of ketone bodies
- Some ketones are acidic resulting in metabolic acidosis
- Impaired brain function can lead to diabetic coma/death

Hypoglycaemia
- Plasma glucose below normal physiological range
- Most often caused by insulin overdose - also insulinoma
- Treated by oral/IV glucose
- Ruminants less sensitive to hypoglycaemia

115
Q

Glucagon

A

Peptide hormone released in response to decreased levels of glucose + amino acids

Overall catabolic effect

Produced in pancreatic ⍺-cells
- Synthesised as pre-pro-hormone
- Converted to pro-glucagon
- Plasma half-life of 5-6 mins
- Deactivated by metabolism in liver/kidneys

116
Q

Regulation/actions of glucagon

A

Stimulated by decrease in plasma glucose
- Also by increase in plasma amino acids + increased sympathetic activity

Binds to receptors on target cells - activates adenyl cyclase

Actions are reverse of insulin
- Net effect on metabolism depends on ratio of insulin: glucagon

Increases plasma glucose by stimulating liver glycogenolysis and gluconeogenesis

Little effect on any tissues other than liver

117
Q

Gross anatomy of liver

A

Located in the dome of the diaphragm within the abdominal cavity

Basic liver has 4 lobes
- Left, quadrate, right % caudate
- In dog, cat, pig, left&right lobes split into medial and lateral parts
- Caudate lobe has 2 parts - caudate + papillary processes

Gallbladder
- Present in carnivores, ruminants, pigs, mice
- Absent in horses, rats.

118
Q

Liver histology

A

Liver surrounded by capsule of connective tissue

Capsule extends into liver as septae - highly branched

Septae delineate the structural units of the liver = hepatic lobule

119
Q

Hepatocytes

A

Chief functional cells of liver

Absorb molecules from “space of disse” - absorption occurs across sinusoidal membrane

Bile canaliculus is dilated intercellular space between cells - bile secreted across canalicular membrane

120
Q

Biliary system

A

Conveys bile from to duodenal lumen

Secrete bile across hepatocyte membrane into canaliculi

Bile flows from canaliculi into small bile ducts = ductules

Ductules anastomose into larger ducts

Ducts coalesce to form hepatic bile ducts

Hepatic bile ducts lead into common bile duct

Common bile duct enters duodenum at Sphincter of Oddi

If present, bile moves between gallbladder & bile duct via cystic duct

121
Q

Blood supply of liver

A

Hepatic portal vein
- 75% of blood entering liver

Hepatic artery
- 25% of blood entering liver

Sinusoids
- Venous + arterial blood mix as they flow into sinusoids

Central veins
- Blood from sinusoids empty into central veins

Hepatic veins
- Central veins coalesce into hepatic veins

Caudal vena cava
- Hepatic veins empty into caudal vena cava

122
Q

Hepatic lobule

A

Hexagonal in shape

Lobules made of plates of hepatocytes

Hepatocytes radiate outwards from a central vein

Between the lobules are portal tracts (triads)
- Bile duct
- Hepatic artery
- Hepatic portal vein

123
Q

Hepatic Acinus

A

= Functional unit of liver

Can be divided into zones

Zones correspond to distance from arterial blood supply

Cells in zone 1 (nearest to artery) best oxygen supply

Cells in zone 3 (furthest from artery) poorest oxygen supply

124
Q

Sinusoids

A

Considered as vascular channels

Lined with fenestrated endothelial cells

Surrounded by layers of hepatocytes

Macrophages (Kupffer cells) patrol sinusoids

Blood flow from portal vein/artery through sinusoids towards central vein

125
Q

Functions of the liver

A

Detox of body wastes, xenobiotics and drugs

Synthesis of cholesterol + bile acids

Synthesis of plasma proteins

Breakdown of RBC (degradation of haem)

Carbohydrate, lipid + amino acid metabolism

Removal of bacteria

Production of clotting factors

Storage of glycogen, iron, copper and vitamins

126
Q

Liver metabolism

A

Carbohydrate metabolism
- Glycogenesis
- Glycogenolysis
- Gluconeogenesis

Lipid metabolism
- Oxidation of fatty acids + ketone body formation
- Synthesis of cholesterol,
phospholipids & bile acids

Protein metabolism
- Deamination + transamination of amino acids
- Synthesis of non-essential amino acids

127
Q

Detoxification + clearance (liver)

A

Major role in purification, transformation and clearance
- All substances absorbed from GI organs pass through liver via hepatic portal vein

Removes harmful substances from blood

Converts substances into less toxic compounds

Hepatocyte microsomes contain non-specific enzyme cytochrome P450 followed by further degradation
- Conjugated with water-soluble compounds and excreted in bile

128
Q

Detoxification and clearance 2 (liver)

A

Drugs (pharmaceuticals)
- Nearly all drugs are modified/degraded in liver
- Conjugated or modified for excretion in urine or bile

Toxins
- Responsible for detoxifying chemical agents + poisons
- Acute/chronic poisoning

Endogenous Metabolites
- Ammonia converted to urea + excreted in urine
- Hormones inactive by liver
- Haem broken down into bilirubin and excreted in bile

129
Q

Examples of Plant toxins

A

Digitalis
- From digitalis purpurea (floxglove)
- Cardiac glycoside

Aflatoxin
- From aspergillus fungus growth on damp grain/soybeans

Phylloerthrin
- Metabolite of chlorophyll
- Causes photosensitzation in sheep

130
Q

Degradation of Red blood cells

A

RBCs removed from blood by macrophages in spleen + liver

Degraded to yield haem from haemoglobin

Haem converted to bile pigments
- Haem converted to biliverdin (green) in macrophage
- Biliverdin transformed to bilirubin (yellow)
- Bilirubin transported to liver in blood bound to albumin
- Bilirubin conjugated with glucoronic acid in liver

131
Q

Excretion of bile pigments

A

Bile pigments play no part in digestion = waste route to haem

Conjugated bilirubin excreted into bile

In gut bilirubin can be acted on by intestinal bacteria
- Remove glucoronic acid
- Metabolise to stercobilin (brown)
- This is what gives faeces its colour

132
Q

Functions of bile

A

Promotes hydrolysis by lipases (effective detergent)
- Bile acids facilitate digestion of dietary triglycerides by acting as emulsifying agents - render fats accessible to pancreatic lipases

Facilitates intestinal absorption of lipids
- Bile acid micelles improve solubilisation and uptake of lipids

Exit route for waste products and drugs
- Synthesis and subsequent excretion in the faeces and represents only significant mechanisms for the elimination of XS cholesterol

133
Q

Composition of bile

A
  • Water
  • Electrolytes
    • bicarbonate actively secreted into bile
  • Biliary proteins
  • Bile pigments
  • Cholesterol
  • Phospholipids
  • Bile acids
    • Cholic acid
    • Chenodeoxycholic acid
134
Q

Storage of bile

A

Bile stored in gallbladder

Allows storage + concentration of bile

Beneficial to animals with intermittent digestion:
- Carnivores
- Omnivores

Herbivores with continuous digestion:
- Levels of fat in diet usually low
- Horses - lack gallbladder
- Ruminants - have gallbladder with ineffective concentrating mechanism - due to presence of fermentation chamber occurring before duodenum probably intermittent rather than continuous

135
Q

Conjugation of bile acids

A

2 major bile acids synthesised from cholesterol in liver
- Cholic acid
- Chenodeoxycholic acid

These bile acids are hydrophobic

To make them water soluble they are conjugated with glycine/taurine
- Cholic acid + glycine = glycocholic acid
- Cholic acid + taurine = Taurocholic acid
- Chenodeoxycholic acid + glycine = Glycochenodeoxycholic acid
- Chenodeoxycholic acid + Taurine = Taurochenodeoxycholic acid

136
Q

Secondary Bile Acids

A

Following participation in lipid digestion/absorption primary bile acids move into ileum

In terminal ileum some primary bile acids can be modified by bacteria

Deconjugated and converted into secondary bile acids
- Cholic acid -> deoxycholic acid
- Chenodeoxycholic acid -> lithocholic acid

137
Q

Summary of bile acids

A

Primary bile (synthesised in liver)
- Glycocholic acid
- Taurocholic acid
- Glycochenodeoxycholic acid
- Taurochenodeoxycholic acid

Secondary bile acids (metabolisation of primary bile acids by bacteria)
- Lithocholic acid
- Deoxycholic acid

138
Q

Bile acid secretion

A

Bile acids transported into bile canaliculus
- This is an active process
- Performed by bile acid transporter protein ATP-driven bile excretory pump (BSEP)

Bile canaliculi isolated from hepatocyte cell membrane by tight junctions to prevent leaks

Bile canaliculi feed into large canals

Bile emptied into duodenum at major duodenal papilla
- Controlled by circular collection of smooth muscle (sphincter of Oddi)

Bile salts not fat soluble so remain in SI lumen until actively reabsorbed in ileum

139
Q

Enterohepatic circulation

A

Bile acids absorbed from terminal ileum by active transport

Transport back to liver via hepatic portal vein

Efficiently captured from blood stream by liver via Na+ dependent Taurocholate co-transport polypeptide (NTCP)

This recycling process referred to enterohepatic circulation

140
Q

Regulation of Bile secretion

A

Parasympathetic Sytem (vagus)

CCK
- Released in response to presence of fat in duodenum
- Causes contraction of gall bladder + relaxation of sphincter of Oddi
- Animal without gallbladder have inactive sphincter of Oddi with continuous flow of bile into duodenum

Secretin
- Released in response of acid chyme in duodenum
- Mainly stimulates release of pancreatic juice
- But also increase HCO3- production by liver

141
Q

Regulation of bile secretion

A

Also regulation by amount of bile salts returning to liver via enterohepatic circulation

During a meal, presence of fat in duodenum causes release of CCK
- Contraction of gallbladder
- Relaxation of Sphincter of Oddi
- Enterohepatic circulation of bile salts increases
- Consequent increase in bile secretion by liver

Between meals lack of fat in duodenum
- Relaxation of gallbladder
- Contraction of Sphincter of Oddi
- Enterohepatic circulation of bile salts decreases
- Bile stored and concentrated in gallbladder

142
Q

Hepatic dysfunction + disease

A

Numerous causes of liver disease in animals
- Infection
- Poisoning (acute/chronic)
- Tumours

Onset of liver disease may affect its major functions
- Bile acid recycling
- Detoxification
- Metabolic functions

Liver has potential to regenerate
- Some disease is reversible

143
Q

Clinical signs of liver disease

A
  • Hepatic dysfunction
  • Depression, low appetite
  • Lethargy
  • Stunting + weightloss
  • Vomiting + diarrhoea
  • Polyuria/polydipsia
  • Ascites + altered liver size
    • hepatomegaly
    • microhepatica
  • Icterus = jaundice
    • Increased bilirubin in blood
  • Bleeding tendancy
144
Q

Clinical biochemistry

A

Liver enzymes released into blood when liver is damaged
- Cats/dogs
- Alanine aminotransferase
- Aspartate aminotransferase
- Horses/ruminants
- Gamma glutamyl transferase
- Alkaline phosphatase

Detection of levels of liver metabolites
- Pre/post-parandial bile acids
- Serum bilirubin
- Serum proteins

145
Q

Cholestasis

A

Intrahepatic
- Decrease in secretion of bile by hepatocytes
- Causes include infections
- Decreased bile flow and back flow of biliary consituents
- Impairs normal biochemical processes within hepatocytes

Extrahepatic
- Obstruction of gallbladder and/or bile ducts
- Causes include tumour, gallstones or inflammation of gallbladder
- Major clinical sign = jaundice

146
Q

Porto-systemic shunts

A
  • Aberrant vessels
  • Connect portal circulation to caudal vena cava
  • Blood bypasses liver
  • 2 main types
    • Congenital = single shunt
    • Acquired = multiple shunts due to portal hypertension
147
Q

Porto-systemic shunts: clinical signs

A

Liver unable to detoxify waste products = hepatic encephaly
- Hyperammoniaemia
- Depression/tremors
- Head pressing

Polyuria/polydipsia

Worse after eating

148
Q

Porto-systemic shunts: diagnosis + treatment

A

Ultrasound, ex lap, fluroscopy
Prognosis:
- Acquired = poor
- Congenital can be corrected by surgery

149
Q

Absorptive State (metabolism)

A

Cells use absorbed nutrients as source of energy + for protein synthesis

Liver takes up glucose/amino acids, fills glycogen stores, synthesises lipids for export to other tissues

XS CHO, fat + protein stored as lipids/glycogen

Net synthesis of protein in all cells

150
Q

Carbohydrate

A

Carnivores/omnivores
- CHO absorbed as monosaccharides, principally glucose
- Galactose/fructose converted to glucose in liver

Herbivores
- CHO fermented to VFAs

Plasma glucose levels maintained at fairly constant level of 5 mmol/l
- In absorptive state, glucose removed from blood + stored + metabolised
- In post-absorptive state stores released

151
Q

Fate of glucose

A

All tissues
- Glucose used as energy source

Liver
- Glucose taken up/stored as glycogen
- This continues until glycogen represents ~5% total liver mass
- Remaining glucose converted into triglycerides
- some stored in liver
- most exported to blood as VLDL

Skeletal muscle
- Glucose taken up/stored as glycogen

Adipose tissue
- Glucose taken up + converted to glycerol for synthesis of triglycerides
- If glucose in XS converted to FFA

152
Q

Lipids

A

Water insoluble so can’t be transported in blood

Made water soluble by binding to proteins
- FFA bound to albumin
- All other lipids bound to apoproteins
- To form lipoprotein
- Apoproteins form interface between lipid core + aqueous blood (similar to bile acids) enabling transport in blood
- 4 major types:
- Chylomicrons
- VLDL
- LDL
- HDL

153
Q

Fate of lipids

A

Chylomicrons + VLDL
- Converted to FFA by lipoprotein lipase
- Taken up by adipose tissue or muscle
- Chylomicron remnants + some VLDL remnants taken up by liver + metabolised
- Remaining VLDL converted to LDL + transfer cholesterol to other cells (bad cholesterol)

HDL (synthesised in liver)
- Transfers apoproteins to chylomicrons + VLDL to enhance lipid uptake
- Remove cholesterol from other cells + transfers it to liver (good cholesterol) as cholesterol-rich HDL
- Cholesterol-rich HDL degraded + releases cholesterol - converted to bile salts or excreted in bile

154
Q

Amino Acids

A

Liver keeps systemic level of amino acids constant

Most (75%) absorbed amino acids taken up by liver via hepatic portal vein
- Used for protein synthesis
- Albumin, fibrinogen, enzymes
- Converted to keto acids
- Provide energy to liver cells
- Converted to glucose/glycogen
- Converted to fatty acids
- Used to synthesise non-essential amino acids

Some (25%) bypasses liver + enters systemic circulation
- Used for protein synthesis
- Used for energy if glucose for storage

Degradation of amino acids for energy leads to NH3
- Converted to urea by liver + excreted by kidneys
- EXCEPT herbivores
- Urea transferred to forestomach/LI via diffusion across epithelium or secreted in saliva (ruminants only)
- Used for microbial protein synthesis
- XS urea excreted by kidneys

155
Q

Post absorptive state (metabolism)

A

Dependant on mobilisation of stored substrates for energy

Liver maintains plasma glucose levels constant by:
- Mobilising glycogen stores
- Producing glucose from other sources (gluconeogenesis)

Use of glucose for energy reserved for brain, erythrocytes, kidneys
- Under anaerobic conditions skeletal muscle also entirely dependent on glucose for energy

Other tissues derive energy from lipids (glucose-sparing)

In pregnancy/lactation glucose essential for foetal metabolism/lactose synthesis hence maintenance of plasma glucose levels in post-absorptive state especially important

156
Q

Mobilisation of glycogen

A

During post-absorptive state no glucose being absorbed

Uptake of glucose by liver stopped

Other tissues continue to use glucose so plasma glucose declines

Liver responds by:
- Reducing its anabolic activities
- Mobilising glycogen stores to release glucose into the blood

Glycogen stores relatively small
- Only sufficient to maintain plasma glucose levels for a few hours

157
Q

Gluconeogenesis

A

As glycogen stores depleted glucose synthesised from non-carbohydrate sources

Performed by liver and kidneys

Substrate is pyruvate
- Formed from lactate, glycerol or amino acids

Many glycolysis enzymes also function in gluconeogeneis

Glucose concentration determines whether glucose converted to pyruvate or vice versa

All animals dependent on glucose but only omnivores absorb sufficient glucose directly from diet

Carnivores
- Diet low in CHO so dependant on gluconeogenesis from digested fat/protein

Herbivores
- CHOs fermented to VFAs
- Only propionic acid can serve as glucose pre-cursor in gluconeogensis

During starvation, glucose pre-cursor is amino acids form animal’s own skeletal muscle

158
Q

Role of skeletal muscle

A

Glycogen stores in skeletal muscle similar to muscle

In post absorptive state skeletal muscle also starts glycogenolysis
- BUT can’t dephosphorylate GP ; free glucose can’t be transported into bloodstream
- Instead glucose oxidised to pyruvate/lactate
- Converted to glucose by liver and can enter bloodstream
- Referred to as Cori cycle

When skeletal muscle glycogen stores depleted amino acids from protein degradation serve as major pre-cursors for gluconeogenesis

159
Q

Use of lipids as energy source

A

During absorptive state VLDL synthesised form XS glucose

During post-absorptive state VLDL synthesised from plasma FFA
- FFA normally transported in blood bound to albumin
- Amount of albumin limits transport of FFA
- FFA transport capacity increased by synthesis of VLDL

VLDL especially important in mobilisation of triglycerides from adipose tissue
- Triglycerides broken down by hormone-dependant lipase
- Glycerol used in gluconeogenesis
- FFA oxidised for energy production (glucose sparing)
- Nervous tissue + foetuses have very low uptake of FFA so heavily dependant on glucose for energy

160
Q

Ketone Bodies

A

Much mobilised FFA taken up by liver

Converted to Acetyl CoA and used as energy source by liver

Most acetyl CoA is surplus + converted to ketone bodies
- β-hydroxybutyrate <> aceto-acetate -> acetone + CO2

Liver can’t re-convert ketone bodies to acetyl CoA for energy production via citric acid cycle but some other tissues can

Monogastric animals:
- Ketone bodies synthesised in pigs/horses (most FFAs re-esterified to triglycerides)
- Brain can switch to ketone bodies as energy source enabling mobilised proteins to last longer

Ruminants:
- Ketone bodies also synthesised from butyrate in ruminal epithelial cells
- important as butyrate inhibits gluconeogenesis from pyruvate
- Unable to limit brain glucose utilisation

161
Q

Regulation of carbohydrate metabolism

A

Insulin (predominates in absorptive state)
- Increased uptake of glucose
- Stimulates glycogenesis
- Inhibits glycogenolysis
- Increases use of glucose for ATP production
- Inhibits glujconeogeneis

Glucaogn (predominates in post-absorptive state)
- Opposite effects to insulin

Adrenaline
- Stimulates glycogenolysis in liver
- Maintains plasma glucose constant despite increased glucose consumption
- Responsible for hyperglycaemia when stressed

Glucocortosoids (^ during starvation)
- Permissive role in gluconegenesis

162
Q

Regulation of protein metabolism

A

Insulin (absorptive state)
- Increased amino acid uptake
- Increased protein synthesis in liver and muscle (anabolysis)

Glucagon (post-absorptive state)
- Increased amino acid uptake in liver only
- Proteins degraded to amino acids that can be used in glucogneogeneis

163
Q

Regulation of fat metabolism

A

Insulin (absorptive state)
- Triglycerides synthesised from glycerophosphates/FFA + stored
- Inhibition of FFA release into blood

Glucagon (post absorptive state + during exercise)
- ^ lipolysis in adipose tissue
- Mobilisation of triglycerides for ATP production

164
Q

Comparative metabolism

A

Insulin:glucagon determines net effect
- Absorptive state - high ratio
- Post absorptive state - low ratio

Ruminants require gluconeogenesis to occur in both absorptive + post-absorptive state as primary source of energy is VFAs not glucose
- Propionic acid/amino acids serve as pre-cursor for glucose in absorptive state
- Amino acids/glycerol serve as pre-cursors for glucose in post-absorptive state
- Utilisation/production of glucose reduced
- Proteins/lipids mobilised
- Insulin:glucagon remains relatively low + constant

165
Q

Carnivores adaption to diet

A

Dog/cat

  • Predators/scavengers
  • High energy content
  • Easily digestible
  • Simple digestive tract
  • Long interval between short meals
  • Spacious stomach for storage
166
Q

Ominvore adaptation to diet

A

Pigs/bears

Best of both worlds

Diet consist of plant/animal origin

Large species variation in digestive tract
- Bears range from herbivore to carnivores
- Degree of fermentation occurs in LI

167
Q

Herbivore adaptation to diet

A

Ruminants/horses

  • Browsers or grazers
  • Low energy content
  • Microbial digestion
  • Digestive tract adapted for fermentation
  • Continuous eating
  • 2 digestive strategies
    • Foregut fermenters
    • Hindgut fermenters
168
Q

Fermentation

A

Non-hydrolysable carbohydrate requires anaerobic, microbial degradation

Long, slow process

Digestive tract adapted:
- To allow microbial population to thrive
- To ensure slow transit of food to allow fermentation

169
Q

Foregut fermenters

A

Ruminants

Stomach modified into fermentation chamber

Very efficient fermentation

Fermentation products absorbed in stomach

Microbial protein can pass into abomasum + SI for digestion/absorption

170
Q

Hindgut fermenters

A

Horses/rabbits

LI modified into fermentation chamber

Moderately efficient fermentation

Fermentation products absorbed in colon

Microbial protein lost in faeces
- Rabbits practice coprophagy

171
Q

Comparative fermentation

A

Hindgut fermentation 70% as efficient as foregut fermentation
- Microbes less efficient
- Less amylolytic fermentation
- Hindgut fermenters lose microbial protein in faeces

BUT
Gut transit time in foregut fermenters dependent on rate of fermentation and can’t be reduced according to nutrient quality of the fibre

Horses on abundant poor quality forage can decrease gut transit time and consume more
- Ruminants more efficient on good quality forage
- Horses ore efficient on abundant poor quality forage
- If forage is in short supply, ruminants predominate

172
Q

Ruminant nutritional strategies

A

Fruit, seeds, buds, young + leaves high in hydrolysable carbohydrate (simple sugars)

Stems, blades, older leaves high in fibre (complex carbohydrates)

Ruminants have 3 nutritional strategies:
- Browsers (concentrate selectors)
- e.g smallest ruminants, giraffes, most deer
- Grazers (grass/roughage eaters)
- e.g cattle, sheep, hippos
- Intermediates (adaptable feeders)
- e.g goats, elk, moose, reindeer, camels

173
Q

Browsers ruminant adaptation

A

Narrow muzzles

More mobile lips/tongue

Smaller forestomach

Ruminant browsers retain functional oesophageal/ventricular groove

SI glucose absorption remains high

174
Q

Grazers ruminant adaptation

A

Wide muzzles

Less mobile lips/tongue

Larger forestomach

Ruminant grazers lose functional oesophageal/ventricular groove

SI glucose absorption declines

175
Q

Oesophageal/ventricular groove

A

Present in all young ruminants

Enables milk to bypass fermentation chamber

Grazer ruminants lose groove function by weaning

Browser ruminants retain groove function to allow diet high in hydrolysable carbohydrate to escape fermentation
- Normal digestion/absorption of hCHO yields more energy than fermentation

176
Q

Herbivore glucose absorption

A

SI is site of glucose absorption via SGLT1

SGLT1 is regulated by diet
- High in young, declines in grazers at weaning
- Remains high in browsers

177
Q

Comparative digestion

A

Carnivores
- No salivary amylase
- High levels of enzymes from stomach/pancreas for proteins + fat

Omnivores
- High levels of salivary amylase
- High levels of enzymes from stomach/pancreas for proteins, fat + carbohydrate

Simple stomached herbivores
- Moderate levels of enzymes for carbohydrate prior to fermentation in LI
- Exploited in feeding concentrate diets high in hCHO

Ruminant herbivores
- Low levels of enzymes for carbohydrate after fermentation in forestomach
- Moderate levels of enzymes for protein digestion of microbial protein in abomasum/SI

178
Q

Comparative absorption

A

Carnivores/omnivores
- Monosaccharides/peptides/monoglycerides + fatty acids absorbed in SI

Simple stomached herbivores
- Monosaccharides/peptides absorbed in SI
- VFA absorbed in LI

Ruminant herbivores
- VFA absorbed in forestomach
- Peptides absorbed in SI

179
Q

Deglutition

A

Swallowing

180
Q

Regurgitation

A

Passive transfer of stomach contents to oral cavity for re-mastication

181
Q

Re-mastication

A

Additional chewing of fibrous material that has been regurgitated

182
Q

Rumination

A

The entire process of regurgitation, re-mastication and re-deglutition

183
Q

Ruminant adaptation to diet

A

Ruminant stomach adapted for fermentation of roughage/fibre

Enlargement of the oesophageal area = forestomach (3 compartments)
- Reticulum
- Rumen
- Omasum

Fourth compartment equivalent to simple stomach
- Abomasum

184
Q

Reticulum/rumen

A

Reticulum
- Inner surface raised to ridges
- Strong wall (smooth muscle)
- Capacity = 10-20 litres

Rumen
- Longitudinal groove/pillar divides it into dorsal + ventral sac
- Walls contain smooth muscle for contraction
- Papillae
- Absorption of H2O, VFAs, ion
- Papillae increase SA:V
- No smooth muscle immobile
- Neural plexuses
- Regulate contraction via short reflexes (within stomach wall)
- Modified by long reflexes (via vagus)

185
Q

Histology of forestomach wall

A

Stratifiet squamous epithelium
- Stratum corner (keratinised layer)
- Stratum granulosum (tight junctions to limit diffusion)
- Stratum basale (cell division occurs, cells migrate towards lumen)
- Capillaries (absorption of diffused substances, blood flow increases 3-4x after feeding)

186
Q

Omasum

A

Located on right side

Reticulo-omasal orifice regulates passage of fermented material from rumen

Multiple leaves with papillae
- Increase surface area
- More leaves/papillae in grazers cf browsers

187
Q

Abomasum

A

Functions like true stomach

Columnar epithelium with glands
- HCl
- Pepsinogen
- Rennin (young ruminants)
- Ppts/coagulates casein
- Retains milk in abomasum longer for action of pepsin

Receives fairly constant flow of fermented material from omasum
- Distension inhibits rumino-reticular contractions
- Regulation of emptying as in simple stomach

pH slightly higher than simple stomach due to alkalinity of fermentation fluid
- Still low enough to kill ruminal microbes for digestion

188
Q

Distribution of digestive components

A

Forage must be reduced in size to allow microbial fermentation

Distribution of forage in rumino-reticulum of grazers depends on density
- Very dense particles (stones/wire) fall straight into reticulum where they usually remain
- Density of other particles depends on associated gas from their fermentation
- Large particles float in bottom of dorsal sac at level of oesophagus
- More dense particles sink into reticulum/cranio-dorsal blind sac/ventral sac
- Gas from fermentation collects at top of dorsal sac

Distribution in browsers less defined as more homogenous + rapid fermentation occurs throughout rumino-reticulum

189
Q

Rumino-reticulum contraction

A

3 types

Primary (mixing of contents)
- 5-8 strong contractions/5 mins during eating
- 4-5 contractions/5 mins during rumination
- 0-1 weak contractions/5 mins during fasting

Secondary (eructation)
- Occur after every 2-3 primary contractions

Rumination
- Extra reticular contraction precedes primary contraction

190
Q

Primary contractions

A

1) First reticular contraction
- Coarse material towards central/dorsal rumen

2) Second reticular contraction
- Fermented material into cranial blind sac
- Small volumes fermented material through reticule omasal orifice into omasum

3)
Cranial blind sac contraction
- Moderately fermented material passes into dorsal sac
- Well fermented material passes into reticulum
Dorsal sac contraction
- Backward contraction
- Overall circular movement of contents in dorsal sac
- Some exchange with ventral sac

4) Ventral sac contraction
- Backward contraction
- Overall circular movement of contents in ventral sac
- Some exchange with dorsal sac
- Well fermented material spills over into cranial blind sac

191
Q

Summary of primary contractions

A

1) First reticular contraction
- Coarse material to dorsal sac

2) Second reticular contraction
- Fine material to cranial blind sac
- FIne materiał to omasum

3) Dorsal rumen contraction
- Fine material from cranial blind sac to reticulum
- Coarse material circled
- Some exchange with ventral sac

4) Ventral rumen contraction
- Fine material circled
- Some fine material into cranial blind sac
- Some exchange with dorsal sac

192
Q

Rumination contractions

A

Rumination occurs when coarse material stimulates oesophageal opening

An extra reticular contraction precedes the normal biphasic reticular contractions

Normal primary contractions then follow

Rumination occurs 6-10 times a day requiring ~60 mins/kg roughage eaten

Rumination generally occurs at night and during afternoon rest period

Ruminants need to ruminate

193
Q

Rumination

A

Newly swallowed material forced into dorsal sac and replaced by partial fermented material

Thorax expands generating -ve pressure in oesophagus

Lower oesophageal sphincter opens

Diaphragmatic muscle contractions force material into oesophagus
- cf abdominal contractions in vomiting

Reverse peristaltic oesophageal contractions convey material to oral cavity

Liquid immediately re-swallowed

Rest of material re-chewed with addition salivary secretion and re-swallowed

194
Q

Contractions with eructation (secondary contractions)

A

2000-4000 litres gas from fermentation per day

Occurs after 2-3 primary contractions

Oesophageal opening usually below level of gas; gas can’t escape during rumination

Eructation can’t occur with animal lying on side
- Makes general anaesthesia/surgery complicated

195
Q

Eructation

A

Primary contractions occur as normal

Caudo-dorsal blind sac contracts forward displacing contents into relaxed cranial blind sac and ventral sac

Dorsal sac continues contraction and moves gas at top of dorsal sac to oesophageal opening
- Increased -ve pressure in thorax causes oesophagus to expand
- Cardiac sphincter opens and gas escapes into oesophagus, reverse peristalsis carrying gas to oral cavity
- Some escapes via mouth but most inhaled

Ventral sac contraction allows gas collecting in caudal-ventral blind sac to escape to the top of the dorsal sac of the rumen

196
Q

Bloat

A

Failure to eructate results in bloat
- Complete oesophageal obstruction
- Partial oesophageal obstruction
- Fresh clover results in small bubbles that fail to coalesce, form a foam that doesn’t collect in the dorsal sac so can’t be eructated

Increased ruminal pressure causes respiratory/caardiac distress

Stretching of rumen reduces/stops ruminal contractions

197
Q

Regulation of forestomach mobility

A

Occurs mainly by autonomic long reflexes

Both afferent + efferent fibres travel in vagus
- Vago-vasal reflex

2 types of sensory cell containing:
- Tension receptors
- Mechano + chemo-receptors

198
Q

Regulation of forestomach motility 2

A

Stimulation - tension receptor containing cells
- In series with smooth muscle cells + sensitive to moderate stretch of rumen walls
- Concentrated around oesophageal opening, oesophageal groove, reticulum wall, rumen pillars + cranio-dorsal blind sac wall
- Increase motility

Inhibition - Mechano/chemorecptor containing cells
- Sensity to severe stretch, pH, osmolarity + VFA concentration
- Located in basal layer of rumen epithelium
- Decrease motility

199
Q

Normal increased motility of forestomach

A

Moderate distension of forestomach

Sensed by tension receptor containing cells

Motility + rumination increased

Food particles broken down more quickly

Sub-group of sensors around reticule-omasal orifice
- Release vasoactive intestinal peptide
- Relaxation of reticulo-omasal sphincter during 2nd reticular contraction

Increases rate of passage of food

200
Q

Normal decreased motility of forestomach

A

Increased [VFA]/increased osmolarity/consequent decreased pH

Sensed by chemoreceptor containing cells

Motility + rumination decreased

Food particles broken down more slowly

Decreases passage rate of food

201
Q

Abnormal motility of forestomach

A

Severe distension
- e.g during bloat

Very low pH <5
- e.g during grain engorgement

Motility decreased

Decreased passage rate of food

202
Q

Central control of forestomach motility

A

Dorsal vagal nuclei in medulla

2 sets of nerve clusters that regulate:
- Frequency of ruminal contractions/rumination
- Force of ruminal contractions

Also recieves input from olfactory organ, tastebuds + oral cavity stretch recptors

Stress causes severe reduction in motility via central control

Strength of ruminal contraction s+ frequency of rumination/ruminal contractions good indicator of general wellbeing

203
Q

Development of forestomach

A

At birth, abomasum developed but not forestomach

Forestomach develops when lamb starts to eat more roughage at ~2-3 wks

Microbes for fermentation develop too but lamb still dependent on milk for nutrition
- Recieved mainly from mother by licking - why bonding so important

Milk bypasses fermentation chamber via oesophageal groove

204
Q

Oesophageal groove

A

Referred to as reticular/ventricular groove

Groove with lops that runs from oesophagus to reticulo-omasal orifice

When animal sucks warm milk, reflex causes lips to curl over forming a tube
- Cold milk prevents complete curling over and can then spill into reticulo-rumen

Milk passes from oesophagus dirct to omasum then abomasum for digestion; avoiding fermentation by developing rumen
- If milk intake>capacity of tube, it spills over into the rumino-reticulum and is fermented
- Lactose rermented to lactate etc
- Adverse effect on developing microbes

Sucking and chemorecptors in pharynx sensitive to milk compounds cause reflex closure of groove
- Can also be stimulated by certain salt solutions used to prepare oral medication that bypasses fermentation chamber

Reflex lost when animal weaned
- Retained if milk is still fed
- Retained in browsers

205
Q

Ruminant fermentation

A

Most plant material can’t b e digested by mammalian enzymes

Requires microbial fermentation
- Ferment food components for their own growth, division + motility
- End products of fermentation used by host

Rumino-reticulum
- Physiologically function together
- Provide environment for microbial population
- Delay gut transit time to allow sufficient time for fermentation

206
Q

Provision of anaerobic environment (for fermentation

A

Oxygen can gain entry to ruminoreticulum from:
- Blood supply
- Swallowed air

Under aerobic conditions, food sustances would be completely broken down to CO2 + H2O which don’t provide energy to the host

Anaerobic contitions prevent total degradation resulting in metabolites that host can use for energy

Certain anaerobic bacteria can use O2 (facultative anaerobes)
- Adhere to luminal surface
- Remove all O2; rendering environment anaerobic

207
Q

Microbes for fermentation

A

Most are bacteria

Protozoa much larger so contribute almost equally to microbial mass

Environment physically/chemically regulated
- Density + competitive balance between microbes remains stable provided feeding pattern is stable
- Too rapid change in ingested food will upset balance

In order to establish microbes must be retained in rumen for sufficient time to allow proliferation
- Ruminal contents are ejected from rumen after fermentation
- Amyolytic bacteria have short lifespan, exist in fluid phase and not retained for long
- Cellulolytic bacteria/protozoa/fungi have longer lifespan so must be retained longer to establish
- Achieve this by adhering to luminal wall/fibre

208
Q

Establishment of ecosystem

A

When newly born gut is sterile

Microbes must be ingested

All environmental microbes are ingested but ruminal ones establish
- Due to rumination mother’s oral cavity contains representative populations of ruminal microbes
- Transferred to young by licking/grooming
- If neotate isolated, will gradually establish bacterial but not protozoal populations

Ruminal microbes adapted to rumen environment so have competitive advantage over other microbes

209
Q

Rumen bacteria

A

Classified on basis of nutrients metabolised

Amylolytic
- Starch/hHCO -> monosaccharides
- High tolerance of low pH
- Can proliferate very quickly at expense of other microbes

Cellulolytic
- Cellulose, hemi-cellulose, fructosans, pectin -> monosaccharides
- Low tolerance of low pH

Proteolytic
- Protein -> Peptides -> amino acids, used for microbial protein synthesis for fermented -> VFAs + NH4+

Methanogenic
- CO2 -> CH4

Lactate-utilisers
- Lactate -> propionate

210
Q

Protozoa/fungi

A

Protozoa
- Mostly ciliates, much larger than bacteria (can engulf bacteria)
- Retained longer in rumen by adhering to large feed particles
- Produce VFAs, lactate, CO2 + H2
- Proliferate with high starch diets, reduced with high fibre diets
- Store glucose as glycogen
- This glucose can be recovered when protozoa pass into SI and are digested
- Ruminants can survive without protozoa but fermentation much more efficient in their presence

Fungi
- Represent small proportion of microbial population
- Reproduce by free-swimming flagellated spores
- Can only break down lignin aerobically
- Rumen under anaerobic conditions
- Lignin indigestible but presumed that spores attach to lignin and split it apart by hyphae, rendering it susceptible to cellulytic digestion
- Proliferate with diets high in lignin

211
Q

Homeostasis of rumen environment

A

Food fermented into metabolites (mainly VFAs + NH4+)

Osmolarity ^/pH decrease

Water enters rumen by osmosis

NH4+ taken up by microbes

VFAs absorbed by host

Increased rumination/HCO3-

Osmolarity lower/pH ^

Water reabsorbed

212
Q

Rumen acidosis

A

Consumption of increased levels of hCHO

VFAs ^^/pH lowered

If pH decreases too much, acid-resistant lactate producers proliferate at expense of lactate utilisers

Lactate poorly absorbed cf VFAs

Too low pH injuries rumen epithelium

Water enters rumen osmosis

Dehydration/hypovolaemic shock ensues

Treated by iv alkaline fluids

Can be prevented by introducing levels hCHO gradually (3-4 wks) to enable lactate utilisers to increase in level with lactate producers

213
Q

Ruminant metabolism

A

Ruminant fermentation very efficient
- Only 10% feed energy lost

Rate of fermentation dependant on
- Type of feedstuff
- Starch fermented more rapidly than fibre
- Volume of feedstuff
- Microbial balance
- Amylolytic bacteria ferment faster than cellulolytic

Homeostatic environment must be maintained by equivalent metabolism of different food components/products of fermentation

Rumen microbes can degrade many toxins before their absorption cf simple stomached animals
- Foxglove leaves (digitalis)
- Ragwort

214
Q

Carbohydrate metabolism (ruminants)

A

Plants contain many different CHO that can be broken down by microbes

Bacterial surface enzymes break down cellulose + starch > monosaccharides/short chained polysaccharides

Dissolved in rumen fluid but not available to host as immediately taken up by microbes and metabolised via glycolysis
- In mammalian cells under aerobic conditions, glycolysis proceeds to CO2 + H20
- As rumen is anaerobic glycolysis can only proceed as far as VFAs

VFAs end products/waste products for microbes but main source of energy for ruminants

Propionate can be formed via 2 metabolic pathways
- Via anaerobic glycolysis of pyruvate
- From lactate

Increased levels of starch enable proliferation of lactate utilisers so high starch diets
- Increase overall VFA production
- Increase relative propionate production

Important as CHO represents 85% total energy from typical diets but only propionic acid (20% total VFA) can be converted to glucose in host cells

215
Q

Methane production (ruminants)

A

CH4 rich in energy

Represents ~10% energy loss from total food energy

BUT
- Glycolysis requires reduction of NAD+
- NAD+ must be regenerated
- Under aerobic conditions in animal cells this ice achieved via respiratory chain
- But rumen environment is anaerobic
- Methane producers reduce CO2 -> CH4 via oxidation of NADH -> NAD+
- Reduce H+ ions; increase pH
- Replenish NAD+ suplies for glycolysis
- NAD+ can also be regenerated by reduction of sulphate/nitrates by other ruminal bacteria

216
Q

Fat metabolism (ruminants)

A

Long chain fatty acids
- Free form
- Triglycerides
- Galacto-lipids

Rapidly hydrolysed galactose/glycerol parts fermented to VFAs (mainly propionic acid)

Most poly-unsaturated fatty acids hydrogenated to mono-unsaturated or saturated fatty acids
- Most common are oleic acid and linoleic acid -> stearic acid

Unsaturated fatty acids synthesised as stereoisomeric cis form in animal tissue

Rumen bacterial hydrogenation also generates some trans unsaturated fatty acids - why ruminant body fat differs to other species

217
Q

Protein metabolism (ruminants)

A

Protein degraded by ruminal bacteria into:
- Peptides
- Amino acids
- NH3 + organic acids
- Branched fatty acids
- Stimulate growth of cellulolytic bacteria

Microbial proliferation requires high rate of protein synthesis
- Mostly derived from inorganic nitrogen
- Also from non-protein nitrogen in food + additives
- Cellulolytic bacteria require NH4+
- Amylolytic use both NH4+ + amino acids

218
Q

Metabolism of non protein nitrogen

A

NPN consists of amides, amines, peptides, amino acids, nucleic acids, urea, nitrates + ammonium ions

Ruminants can utilise NPN for protein synthesis via microbes
- NPN -> NH3 -> amino acids -> protein
- Microbial protein digested in stomach/SI as in simple-stomached animals

NPN essential for healthy microbial population
- Grass/grain contains 5-15% NPN
- Silage contains 70% NPN (due to microbial fermentation)

219
Q

Lactation requirements (ruminants)

A

Ruminants can function normally if nitrogen only supplied as NPN

High producing dairy cows require more than microbial protein
- Urea often added to diets to increase NPN
- Increases microbial population so protein available for digestion
- Microbes must be supplied with extra energy in order to proliferate
- Extra protein added to diets
- Escape fermentation as poorly soluble
- Passes into abomasum/SI for digestion

XS protein recycled into urea and secreted in saliva

XS urea excreted by kidneys
- Energy costly so feed should only contain slightly more NPN than microbes require

220
Q

Absorption (ruminants)

A

Selective transfer of useful nutrients into host’s bloodstream

Reticula-rumen enhances this by papillae, increasing SA
- Papillae most dense in parts of rumen responsible for absorption (ventral sac + cranial/caudal-dorsal blind sacs)

Requires specific transport proteins and energy source

Feed material must be digested to sufficient size to enable absorption
- Mainly VFAs

Monosaccharides/di/tri-peptides/amino acids unavailable to host as immediately taken up by microbes

221
Q

Rumen absorption

A

VFAs
- ~80% total VFAs absorbed
- Stratum corneum permeable to anion/un-dissociated acid
- Stratum glanulosum only permeable to un-dissociated acid
- Rumen pH decreases as fermentation proceeds, un0dissociated form conc increases
- BUT at normal rumen pH anion form predominates
- Postulated that some H+ producing mechanism in epithelium causes local increase in un-dissociated form , enabling absorption
- Acetic acid absorbed unchanged
- Some propionic acid metabolised to lactic acid as absorbed
- All butyric acid metabolised to β-hydroxybutyric acid as absorbed

Water
- Moves between rumen content/ECF depending on osmotic gradient

Lactic acid
- Stronger acid so more poorly absorbed than VFAs
- Tends to remain in rumen, lowering pH
- When absorbed, converted to glucose by liver

Ammonia
- NH4+ prodominates but NH3 rapidly absorbed so equilibrium continually shifting to NH3 form
- When absorbed converted to urea by liver

Inorganic ions
- Rumen -ve reliable to blood - hinders absorption of +ve ions
- Na+/Mg2+ actively transported to blood
- Cl- absorbed in exchanged for bicarbonate
- Ca2+/PO42- mainly absorbed in SI

222
Q

Omasal absorption

A

SA increased by leaves/papillae

Fermentation continues in omasum

Absorption of ~10% total VFA leaving 10% passing into omasum

Water/Na+ also absorbed
- Ingesta so more solid than in rumen
- Contains less HCO3- so abomasum needs to secrete less H+

Some rumen material passes straight into absorption via omasal canal

223
Q

Functional anatomy of the hors

A

Ascending colon castle modified into fermentation chamber
- 3 compartments separated by physiological valves
- Caecum separated from ventral colon by caeca-colic valve - also separated from ileum by ileo-caecal valve
- Ventral colon separated from dorsal colon by narrow pelvic flexure
- Dorsal colon separated from small colon by narrowing transverse colon

Transverse colon relatively short and narrows down to meet descending colon

Longitudinal muscle not continuous strand but arranged into taenial bands
- Different number of taenia in different parts
- Shorter than large intestine itself resulting in sacculations
- Enable mixing and delays transit time to allow fermentation

224
Q

Fermentation (equine LI)

A

Similar process to that occurring in ruminant forestomach

Degree of fermentation depends on material reaching LI
- In carnivores most digestion/absorption has already occurred prior to LI so fermentation minimal
- In ruminants/omnivores, fermentation moderate
- In horses vast majority of non hydrolysable CHO reaches LI so fermentation extensive

Microbial products of fermentation are VFAs/CH4/CO2
- LI mucosa can absorb these VFAs
- Gasses passed to rectum by peristalsis and expelled

Microbial balance can be easily upset, just as in ruminants

As LI is terminal part of GI tract some VFAs and all microbial protein egested/wasted
- Rabbits/rats practice coprophagy to avoid this waste

225
Q

Metabolism of VFAs (Equine LI)

A

Energy sources
- Especially in horse
Homeostasis of colonic epithelium by regulating genes controlling proliferation/apoptosis/differentiation

Acetate
- Used in liver
- Oxidised in most other cells to generate ATP
- Major source of acetyl CoA lipid synthesis

Propionate
- Substrate for gluconeogenesis

Butyrate
- Energy production
- Cellular homeostasis

226
Q

Absorption (equine LI)

A

VFAs (accettate, propionate, butyrate)
- Absorbed by SCFA/HCO3- exchanger

Na+
- Absorbed by Na channels + Na+/H+ exchanger
- Sodium absoption enhanced by aldosterone

Cl-
- Absorbed by bicarbonate/hydroxyl exchange

Water
- Most of water passing from SI absorbed in LI
- Osmotic pressure
- Hydrostatic pressure
- Solvent drag
- Extensive reabsorption in horses

227
Q

Comparative physiology (equine)

A

LI physiology similar in most domestic species except horse

In feral horse on grass diet, 75% energy derived from VFAs produced by microbial fermentation in hindgut

Fermentation similar process to in ruminant forestomach
- BUT SI occurs before fermentation vessel
- In ruminants, any hCHO immediately fermented so none passes into SI
- However in horse potentially lots of hCHO can pass into LI if overload of SI capacity to digest/absorb it

228
Q

Carbohydrate fermentation (equine)

A

Fibre requires microbial fermentation
Products of fermentation are mainly VFAs

VFAs cause a decline in pH of luminal contents
- Neutralised by copious pancreatic secretion containing HCO3-
- Goblet cells in LI secrete mucus + HCO3-
- Ileum also secretes HCO3-

If production of VFAs excessive H= ions too numerous to be neutralised by HCO3- secretions
- pH of luminal contents declines
- Favours multiplication of acid resistant microbes
- Lactic acid poorly absorbed cf CFAs causing further pH decline

229
Q

Protein fermentation (equine)

A

Probably similar to ruminants
BUT
Equine hindgut more capable of absorbing amino acids/peptides
Less amino acids/peptides taken up by microbes, more being absorbed by the host
Good thing as microbial protein is lost in faeces in hindgut fermenters
Microbial nitrogen requirements satisfied by urea secreted by ileum/LI
- Broken down by microbial urease into NH3 to be used as NPN source for microbial protein synthesis

230
Q

Water absorption (equine)

A

Compared to other species more water reabsorption occurs in large intestine

At luminal pH (6.5) most VFAs in ionic form which are poorly absorbed

Local mechanism of secretion of H+ in exchange for Na+ converts ions to their respective acids, enhancing their absorption

HCO3- secreted in exchange for Cl- maintain pH at level suitable for fermentation

Consequently when VFAs absorbed there is also a net absorption of NaCl which enhance water reabsorption via osmotic pressure + solvent drag

231
Q

VFA absorption

A

Compared to ruminants VFAs are absorbed intact rather than metabolised as they’re absorbed

As in ruminants, proportion of propionic acid increases with more hCHO passing into LI
- Substrate for amylolytic bacteria causing their proliferation
- But hCHO mustn’t be fed excessively otherwise it will disturb the microbial balance
- With dietary adaptation SI digestion/absorption of hCHO can increase to prevent overload
- Much more energy efficient to digest hCHO and absorb as glucose rather than ferment it to propionic acid for gluconeogenesis

232
Q

Microbiology (equine)

A

Bacteria
- Food material passing into fermentation chamber generally contains lower levels of hCHO
- Amylolytic population lower so fermentation slower

Protozoa
- Ciliates as in ruminant but different species
- Smaller number than bacteria but larger - contribute similar total mass
- Contribution to fermentation unknown
- If removed, very little difference to fermentation efficiency
- Protozoa lost in faeces so can’t be digested as in ruminant

Fungi
- Probably similar to ruminants
- Split apart lignin, rendering it susceptible to digestion by celluloyti bacteria

233
Q

Foregut vs hindgut fermentation

A

Hindgut fermentation 70% as efficient as foregut fermentation
- Microbes less efficient
- Lower degree of amylolytic fermentation
- Hindgut fermenters lose microbial protein in faeces
- coprophagy - rabbits

BUT

Gut transit time in foregut fermenters dependent on rate of fermentation and can’t be reduced whatever the nutrient quality of the fibre

Horses on poor quality forage can decrease gut transit time and consume more
- Ruminants more efficient on good quality forage
- Horses more efficient on poor quality forage as long as its in abundance

234
Q

Motility (equine LI)

A

Large intestinal transit time must be slow enough to allow fermentation to occur
- Hindgut fermenters - several days
- Foregut fermenters - 24 hours

In most species, caecum + colon form continuous compartment
- In horses, caecum separated from colon by caeco-colic valve
- Separate fermentation compartment with no retrograde flow of material from colon to caecum

235
Q

Caecal contractions (equine)

A

Segmental contractions main type
- Maintains high microbial activity for fermentation + absorption

Mass contractions occur every 3-5 mins
- Coordinated contraction of entire caecum
- Mass evacuation of caecal contents into colon
- Similar to peristaltic contractions but smooth muscle contracts for longer

236
Q

Colonic contractions

A

Most species
- Main contractions are segmental, peristaltic + anti-peristaltic
- Anti-peristaltic contractions more prominent in proximal colon
- Retrograde movement of chyme from colon into caecum

EXCEPT in horse
- No retrograde movement from colon into caecum
- Anti-peristaltic contractions occur principally in distal part of ventral colon
- Slow movement of passage of chyme from ventral to dorsal colon via pelvic flexure
- Only small particle/well fermented material can pass via pelvic flexure into dorsal colon
- Ensures slow enough transit time to allow efficient fermentation

Omnivores/carnivores also have mass movement contractions in colon for evacuation

237
Q

Equine colic

A

Not a disease but a clinical sign of abdominal pain
- True colic - GI pain
- False colic - other abdominal organ pain

Colic results in the highest levels of equine mortality + morbidity so an accurate diagnosis is essential to treat successfully

The most useful procedure in diagnosis is rectal examination

238
Q

Normal sounds in equine abdominal auscultation

A

Left dorsal - SI/small colon
- Fluidy in nature, higher pitch

Left ventral - pelvic flexure

Right dorsal/ventral - caecum
- Loud, toilet flushing sound

239
Q

Abnormal sounds in equine abdominal auscultation

A

Increased frequency
- Enteritis
- Spasmodic colic

Tympanitic
- Gut distension with gas
- Obstruction

Decreased frequency
- Ileus
- Obstruction

240
Q

Normal equine rectal examination

A

Spleen lying against left abdominal wall

Caudal pole of left kidney dorsal and left of midline
- Nephro-splenic ligament/nephro-splenic space palpable between the above

Caecum to right of midline
- Ventral taenia extending from upper right to ventral midline

Aorta in dorsal midline

Root of the mesentary in dorsal midline running ventrally

Pelvic flexure lying left ventral

Small colon containing faecal pellets lying left dorsally
- SI not usually directly palpable unless it contracts during palpation

241
Q

Equine rectal exam - SI obstruction

A

Normally can’t feel SI as it is empty

If distended by gas, inicator of obstruction

SI obstruction causes dehydration of large colon contents
- Feels hard + vacuum wrapped
- Distinguish from primary large colon impaction

242
Q

Equine rectal exam - Ileal impaction

A

Firm tubular structure in centre of abdomen coursing towards caecum

If detected early, SI distension minimal

If detected late, SI will be distended

243
Q

Equine rectal exam - Caecal impaction

A

Primary - impaction with ingesta

Secondary - to obstruction of large colon

Taenia become more taut

Caecum displace more to midline

244
Q

Equine rectal exam - Colonic impaction

A

Most commonly occurs at pelvic flexure

Obvious palpable mass in left ventral quadrant
- Large colon feels enlarged

Usually can be treaded medically
- cf secondary impactions

245
Q

Equine rectal exam - Left dorsal displacement

A

Also called nephro/reno-splenic entrapment

Left colon passes to left of spleen and becomes trapped over nephro-splenic ligament

Left colon palpable on left and dorsally

If long-standing left colon becomes too distended to palpate nephro-splenic ligament

246
Q

Equine rectal exam - right dorsal displacement

A

Left colon displaced lateral to caecum

Pelvic flexure usually ends up in left cranial abdomen beyond reach

Caecum displaced cranio-medially and becomes more difficult to palpate

247
Q

Equine rectal exam - large colon volvulus/torsion

A

Abdomen visibly distended

Large colon fills entire abdomen
- Often can’t advance arm into abdomen beyond pelvic rim

Colon markedly distended

Volvulus occurs first but often associated with torsion + consequent vascular compromise

248
Q
A

Liv vet med yr1 (18 decks)

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