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GIT Flashcards

1
Q

What are the 4 basic digestive processes?

A

Mechanical
Secretion
Digestion
Absorption

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2
Q

What are the primary functions of the digestive tract?

A

Transport
Digestion - mechanical and chemical (hydrolysis).
Secretion - via exocrine glands (saliva, enzymes).
Absorption
Synthesis
Excretion

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3
Q

Describe some characteristics of carnivore GIT’s.

A

High energy diet - readily digested.
Short, simple GIT - fast digesta transit.
Large stomach, short small intestine.
Teeth designed for killing, not chewing.

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4
Q

Describe some characteristics of herbivore GIT’s.

A

Natural diet and so low energy digestible energy content.
Long time eating and chewing.
Most CHO breakdown by anaerobic microbial fermentation.
Complex GIT - fermentation
Foregut or hindgut fermenter.

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5
Q

Describe some characteristics of omnivores GIT’s.

A 
More flexible than carnivores and herbivores.
Monogastrics.
GIT of varying length and complexity.
Posterior teeth for grinding.
Anterior teeth for piercing and ripping.
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6
Q

Describe some characteristics of avian GIT’s.

A

Plant material - beak for crushing seeds, large caeca for fermentation.
Animal material - beak for tearing, simpler GIT, small caeca.
All birds have a crop (out pocket of oesophagus for storage).
Glandular and muscular portions to stomach.
LI empties straight to cloaca.

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7
Q

What are the 3 main types of digestive systems?

A

Monogastric
Foregut
Hindgut

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8
Q

How is the GIT regulated?

A

Coordinates digestion, secretion and motility.
Maximise absorption of nutrients.
Acts to maintain favourable conditions in lumen.
Intrinsic and extrinsic control systems.

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9
Q

What is the intrinsic system controlling the GIT?

A 
Located in wall of GIT.
Involves nerves (enteric NS) and endocrine secretions (secretin, gastrin, CCK, GIP, Motilin).
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10
Q

What is the extrinsic system controlling the GIT?

A 
Located outside the wall of the GIT.
Involves nerves (vagus and splanchnic nerves) and endocrine secretions (aldosterone).
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11
Q

What are the two major enteric plexuses (networks of nerves)?

A

Myenteric (Auerbach’s) plexus - ganglia between the circular and longitudinal muscle layers.
Submucosal (Meissner’s) plexus - ganglia between submucosal and circular muscle layers.

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12
Q

What are the 3 parts of the Enteric/Intrinsic NS?

A

Sensory/afferent neurons - mechanoreceptors, chemoreceptors, osmoreceptors (present in mucosa and muscle wall).
Interneurons - connecting neurons between sensory and motor.
Motor/Efferent neurons - smooth muscle GIT wall, glands.

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13
Q

True or false. Neural regulation can be completely independent of external innervation.

A

True

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14
Q

Where are the sensory neurons of the intrinsic NS located?

A

Mechanoreceptors - muscular layers (detects distension of gut wall).
Chemoreceptors - mucosa (detects chemical conditions in gut lumen).
Osmoreceptors - mucosa (sensitive to osmolarity of gut contents).

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15
Q

What are the three motor neurons of the intrinsic NS?

A

Gut smooth muscle neurons - axons end in varicosities that release neuroregulatory transmitter substances (neurocrines).
Stimulatory/excitatory neurons - cholinergic (ACh), peptide transmitters (substance P and K).
Inhibitory neurons - mostly peptide neurotransmitters (eg. somatostatin), some non-peptides (eg. NO, ATP).

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16
Q

How are enteric neurons classified?

A

Morphology (motor, sensory, mixed)
Electrophysiological (fast, longer lasting AP)
Chemical (cholinergic, adrenergic)

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17
Q

How does the extrinsic system influence GIT motility and secretion?

A

Via Autonomic NS (incl PNS and SNS);

  1. Modifies ongoing activity in the intrinsic plexuses.
  2. Altering levels of GIT hormone secretion.
  3. Acting directly on the smooth muscle and glands.
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18
Q

What effect does the PNS have on the GIT?

A

Increases gut blood flow, motility and glandular secretions.

Two components - vagal efferent and afferent (vagovagal reflex).

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19
Q

What is the splanchnic nerve?

A

Celiaco-mesentric ganglia;
1) sympathetic afferents - ganglion in thoracic-lumbar region (pre-ganglion) and calico-mesenteric ganglion (post-ganglion).
2) Spinal afferents - spinal cord (dorsal root ganglia).
Has visceral and spinal afferents.
Signal CNS pathological conditions (colic).

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20
Q

What effect does the SNS have on the GIT?

A

Inhibits gut motility

Increases glandular secretions.

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21
Q

What are some accessory glands of the GIT?

A

Salivary
Pancreas
Liver

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22
Q

Which nervous system is considered the ‘long reflex’? What does it involve?

A

Extrinsic NS.
Stimuli from other parts of body (vision, taste, smell) OR from lumen via sensory cells -> CNS -> Nerve plexuses and accessory glands -> affects motility and glandular secretion of smooth muscle or glands.

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23
Q

Which nervous system is considered the ‘short reflex’? What does it involve?

A

Enteric NS.

Stimulated by sensory cells within lumen -> nerve plexuses -> affects motility and secretions of smooth muscle or glands

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24
Q

What are enterocytes? What are the three main forms?

A

Epithelial cells within GIT.
Absorptive
Endocrine
Exocrine (goblet cells)

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25
Q

What are the gastric exocrine (secrete into lumen) secretory cells?

A

Mucous cells - mucous
Chief cells - pepsinogen (stimulated by ACh, gastrin)
Parietal cells - HCl (stimulated by ACh, gastrin, histamine).

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26
Q

What are the gastric endocrine (secrete into interstitial fluid or blood) and paracrine secretory cells?

A

Enterochromaffin-like cell (ECL) - histamine (stimulated by ACh, gastrin).
G cells (pyloric gland area) - gastrin (stimulated by protein products, ACh).
D cells - somatostatin (stimulated by acid).

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27
Q

What is the intrinsic endocrine system?

A

Extensive number and variety of endocrine cells distributed diffusely through epithelium.
In both secretory and absorptive areas of mucosa (stomach and SI).
Produce regulatory peptides (GI).
Form part of regulatory feedback loops influencing GIT function.

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28
Q

What are the classes of GI peptides?

A

Gastrointestinal peptides.
Endocrine - secretin, gastrin, cholecystokinin (CCK), gastric inhibitory peptide (GIP), motilin.
Neurocrine - vasoactive, gastrin-releasing (GRP), enkephalins.
Paracrine - somatostatin, histamine.
All are required to bind to specific receptors on target cells to illicit response.

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29
Q

How is the GIT involved in the immune system?

A

GI immune system monitors antigenic environment.

Increases gut motility and glandular secretions to dilute and dislodge antigens.

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30
Q

What are the phases of gastrointestinal control?

A

Cephalic
Gastric
Intestinal

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31
Q

What is the cephalic phase?

A

Oral cavity.
Response to food related stimuli in brain (thinking about food, tasting, smelling, chewing).
Long reflex via vagus nerve - increases secretion (HCl, pepsinogen) and motility.

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32
Q

What is the gastric phase?

A 
Stomach.
Occurs in response to food in stomach.
Long and short reflexes.
GIT hormones.
Gastrin released to enhance events of gastric phase.
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33
Q

What is the intestinal phase?

A 
Intestines.
Occurs in response to factors originating in the duodenum after food has left the stomach and entered SI. 
Long reflex, short reflex, GI hormones. 
Secretin and CCK.
Absorption promoted.
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34
Q

Which three hormones control appetite?

A

Leptin
Ghrelin
Peptide YY (PYY)

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35
Q

How is feed intake regulated in the long term?

A

Hypothalamus is main control - ventromedial nucleus is satiety centre and arcuate, paraventricular nucleus, and dorsomedial nucleus all regulate feed intake.
Hormonally - leptin, ghrelin, PYY.

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36
Q

What effect does ghrelin have?

A

Appetite stimulating hormone.

Released from gastric cells when stomach is empty.

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37
Q

What effect does PYY have?

A

Appetite reducing hormone.

Released from enteroendocrine cells when colon is full.

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38
Q

What effect does leptin have?

A

Hormone released from adipose cells that suppresses hunger (via hypothalamus).
When energy intake exceeds demands fat is deposited in adipose tissue increasing the amount of leptin.

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39
Q

Which two peptides secreted by the hypothalamus play a role in long term control of appetite?

A

NPY - substance neuropeptide Y, increases food intake and decreases energy expenditure.
POMC - pro-opiomelanocortin, decreases food intake and increases energy expenditure.
Both released in arcuate nucleus.

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40
Q

How is feed intake regulated in the short term?

A

Satiety factors - insulin, CCK, neural input from chemo and mechano receptors.
Insulin stimulates leptin synthesis by adipocytes.

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41
Q

What are the two forms of neural control?

A

Extrinsic - autonomic NS

Intrinsic (enteric) - myenteric and sub-mucosal plexus.

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42
Q

Hormones which are secreted into vascular system and transported elsewhere are acting in what manner?

A

Classical hormone - endocrine activity.

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43
Q

Name 3 endocrine peptides?

A

Gastrin
Cholecystokinin
Secretin

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44
Q

Where are neurocrines produced?

A

Released by enteric NS (specialised group of nerve cells) - through varicosities.

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45
Q

What are the differences between cephalic, gastric and intestinal phases of gastrointestinal control?

A

Cephalic - long reflex, increased secretion and motility, preparation of gut for arrival of food.
Gastric - long and short reflexes, presence of food in stomach, release of gastrin.
Intestinal - long and short reflexes, presence of food in duodenum, release of secretin and CCK.

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46
Q

What is the first act of digestion?

A

Mastication.
Initiates mechanical break down.
Reflex response stimulates secretion of saliva, gastric juices, pancreatic juices and bile.

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47
Q

What is deglutition?

A

Swallowing

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48
Q

What are the phases of swallowing?

A

Pharyngeal, cricopharyngeal (no swallowing - upper oesophageal sphincter closed OR with swallowing - vagal inhibition allows relaxation of muscles and bolus enters oesophagus), oesophageal (peristalsis), gastro-oesophageal (passage through sphincter which is normally closed, preventing reflux).

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49
Q

Which mechanisms prevent reflux?

A

Short segments of oesophagus within abdomen act like valve.
Increased abdominal pressure causes oesophageal lumen to close.
Oesophagus enters stomach at sharp angle, becomes more acute with distension.

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50
Q

What are the functions of motility within the GIT?

A

Propel
Retain
Physical breakdown of food and mixing.
Circulate ingesta - increasing contact with absorptive surfaces.

Motility can be propulsive, retentive or mixing in nature.

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51
Q

What does GIT musculature function as?

A

Syncytium. Connected by gap junctions.

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52
Q

What kind of muscle causes motility in the GIT.

A

It is unitary (single unit) smooth muscle.

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53
Q

What are the unique features of GIT smooth muscle?

A

Baseline membrane potential -70 to -60mV.
Intrinsic electrical properties; spontaneous undulating waves or partial depolarisation, membrane potential fluctuates rhythmically (20-30mV), changes propagate aborally along GIT, basal electrical rhythm (BER) dependent on interstitial cells of cajal (ICC - pacemaker cells). Affected by neural activity and hormones.

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54
Q

Do ICC initiate an action potential?

A

No, they generate slow wave potentials that undulate resting membrane potential closer to threshold.

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55
Q

How are slow waves initiated in smooth muscle of the GIT?

A

Interstitial cells of Cajal.
Spontaneous depolarisation caused by variations in sodium conductance.
Located at muscle layer boundaries (submucosa/circular, longitudinal/circular, extend length of gut).
Connected to smooth muscle cells by tight junctions, allowing spontaneous electrical activity to be transferred.

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56
Q

What are slow waves?

A

Rhythmic, wavelike fluctuations in membrane potential that cyclically bring the membrane closer to or further from threshold. Not an action potential.

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57
Q

What are the functions of gastric smooth muscle?

A

Receptive relaxation - relaxes to accomodate food (orad area).
Retropulsion - mixes food with gastric juice (caudad area).
Antral pump - propels chyme into duodenum (caudad area).

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58
Q

Describe gastric motility in proximal stomach.

A

Reservoir to store food, minimal mixing.
Wall undergoes receptive relaxation and adaptive relaxation to accomodate meal (gastric filling).
Tonic contractions push digesta towards antrum and are involved with emptying of liquids.

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59
Q

Describe gastric motility in the distal stomach.

A

Thick muscle with vigorous phasic contractions.
Trituration (grinding), mixing and emptying.
Peristaltic waves start in corpus and move aborally.
As the waves near pylorus it constricts and only allows passage of small particles.

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60
Q

What are the two major processes of gastric motility?

A

Gastric mixing - trituration/retropulsion

Gastric emptying - astral pump

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61
Q

What does the enterogastric reflex control?

A

Gastric emptying by regulating stomach motility.
Different rates for solid and liquid.
Rate of food leaving stomach needs to match rate of digestion and absorption by SI.

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62
Q

What are the 2 phases of digestion within the SI?

A

Digestive

Interdigestive

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63
Q

What are the motility patterns within the digestive phase?

A

Segmentation - mixes and slowly propels chyme, initiated by small intestine pacesetter cells. Frequency decreases the further along the SI you get.
Propulsive - peristaltic contractions, only pass over small segments before they die out.

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64
Q

What occurs within the GIT between meals?

A

Remaining indigestible particles in stomach are removed by relaxation of the pyloric sphincter, powerful waves of peristalsis.

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65
Q

What is the inter digestive motility complex?

A

Occurs at hourly intervals, disrupted by eating.
Powerful waves of peristalsis remove remaining undigested particles from stomach.
Periods of quiescence followed by series of intense peristaltic contractions.

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66
Q

What is the migrating motility complex/migrating myoelectric complex?

A

‘Sweeps’ undigested material along to colon.
May also be involved in controlling bacterial populations in the upper gut.
Peristaltic contractions can sometimes transverse entire organ.

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67
Q

What are the 4 main functions of motility?

A

Propel
Retain
Break down
Circulation

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68
Q

What are prehension, mastication and deglutination?

A

Placing food in mouth, chewing and swallowing.

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69
Q

What occurs when food is present within the stomach?

A

Gastrin is released, this inhibits the ileocaecal sphincter (relaxes it) and allows movement of chyme into caecum and colon.

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70
Q

What are the 3 types of contraction within the LI?

A

Segmentation (haustration) - primary method of motility, role in mixing, non-propulsive.
Peristalsis/antiperistalsis - pacemakers in mid colon region generate slow waves that propel chyme over short distance.
Mass movements - aboral propulsion over long distances.

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71
Q

How is LI motility regulated?

A

Smooth muscle cells have fluctuating membrane potentials due to pacemaker areas however exact mechanisms are not fully understood.
Myogenic activity modulated by nerves and hormones.

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72
Q

What is the gastrocolic reflex?

A

When food enters stomach it causes mass movements in colon.
Mediated by gastrin and extrinsic autonomic NS.
Pushes colonic contents into rectum.

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73
Q

What is the gastroileal reflex?

A

Movement of remaining SI contents into LI.

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74
Q

What is the defecation reflex?

A

LI contents are forced into rectum stimulating stretch receptors.

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75
Q

Why are ruminants called ruminants?

A 
They ruminate (chew cud).
Voluntarily regurgitate partially digested food back into mouth to complete mechanical grinding. 
Rumen houses microbes that break down cellulose and other complex CHO's.
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76
Q

What is the reticular groove reflex?

A

Milk bypasses immature fore stomach (rumen) to enter abomasum.
No longer used after 2-3months of age.

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77
Q

Describe the stages of the reticular groove reflex?

A
  1. Reflex initiated (drinking, sucking).
  2. Milk in pharynx stimulates receptors.
  3. Afferent impulses via trigeminal nerve.
  4. Efferent impulses via vagus.
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78
Q

What are rumen pillars important for?

A

Motility and stability.

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79
Q

What are the functions of the ruminant fore stomach (rumen)?

A 
Storage
Suitable fermentation environment (anaerobic, buffered, 37degrees celsius).
Mixing
Transportation to abomasum.
Eructation.
Rumination.
Absorption of VFA's.
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80
Q

What are the different types of rumen/reticulum contractions?

A

Primary contractions - mixing.
Secondary contractions - eructation of gas.
Rumination contractions.

81
Q

Describe the stages of primary contractions in the rumen and reticulum.

A
  1. Start in reticulum, 1-3per min. Reticular wall contracts twice in 5-10sec, relaxes for 1mins.
  2. Second reticular contraction, almost completely empties reticulum of remaining fine material (back to atrium).
  3. Rumen contraction begins in atrium and cranial pillar, spreads caudodorsally over dorsal sac. Ventral sac raises and moves atrial contents cranially, back to reticulum. Dorsal sac contracts, digesta pushed to caudodorsal blind sac.
    Contraction of blind sac and caudal pillar forces digesta up and forwards (completes circular movement of digesta).
  4. Ventral sac contracts pushing ingest into caudoventral blind sac. Some ingesta also flows to atrium. Moved backwards and forwards between atrium and reticulum, eventually emptying into omasum.
82
Q

Describe the coordination of rumen secondary contractions.

A

May occur after alternate primary cycles.
Fermentation gases are moved cranially and dorsally.
Dorsal rumen contraction reaches atrium, cranial pillar elevates, fluid moved away from oesophagus, allowing gas to enter.
Filling phase - retroperistalsis moves gas into space near oesophagus. Clearing phase - gas exits via oesophagus (eructation).

83
Q

What is the clinical significance of secondary rumen contractions?

A

Ruminal tympany

Bloat

84
Q

What are the 3 main steps of rumination?

A

Regurgitation
Remasticate
Reswallow.

85
Q

How does regurgitation occur?

A

Short reticular contraction that precedes biphasic reticular contraction in primary cycle.
Recently ingested material near oesophageal opening replaced by semi-liquid, partially fermented material.
Lower oesophageal sphincter opens, negative pressure in thorax ‘sucks’ material into oesophagus (anti peristaltic waves propel cud into mouth through upper oesophageal sphincter.

86
Q

Describe the neural innervation of regurgitation?

A

Mainly via long vagovagal reflexes.
Sensory innervation from fore stomach receptors.
Primary and secondary cycles are extrinsic contractions due to vagus.
If no vagal input then no ruminoreticular contractions.
Intrinsic contractions (enteric NS) responsible only for smooth muscle tone of fore stomach.

87
Q

Where will you find stretch receptors in the fore stomach?

A 
Oesophageal opening
Reticular groove
Reticular wall
Rumen pillars
Atrium
88
Q

What is vomiting?

A

NOT reverse peristalsis.
Forceful expulsion of gastric contents due to contraction of respiratory muscles (diaphragm and abdominals).
Coordinated by non-distinct centre in medulla.

89
Q

Does the stomach actively participate in vomiting?

A

No - stomach, oesophagus, oesophageal sphincters and pyloric sphincters are all relaxed.

90
Q

How do ruminants ruminate?

A

Reverse peristalsis.
Striated oesophageal muscle.
Birds also carry out reverse peristalsis to feed young.

91
Q

Describe the events associated with vomiting?

A
  1. Relaxation of stomach, oesophageal sphincter and closing of pylorus.
  2. Contraction of abdominal muscles, increasing intra-abdominal pressure.
  3. Expansion of chest cavity, glottis remains closed (lowers intrathoracic pressure).
  4. Upper oesophageal sphincter opens.
  5. Gastric contents expelled by contraction of abdominal muscles and diaphragm. Stomach is squeezed due to pressure changes.
92
Q

What are the different secretions of the GIT?

A

Salivary - Mucin, serous, amylase.
Gastric secretions - acid, proteolytic enzyme (pepsin), mucin.
Pancreatic secretions - sodium bicarb, amylolytic enzymes, proteolytic enzymes, lipolytic enzymes.

93
Q

What are the 2 types of saliva secretions?

A

Viscous/Mucous - mucous rich, from small glands, contains mucin for lubrication.
Serous - parotid glands, watery secretion containing amylase.

94
Q

What are the 4 salivary glands and their main secretions?

A

Parotid - Serous
Submandibular - Mucous, serous
Sublingual - mucous, serous.
Buccal - mucous

95
Q

What is saliva and what is its purpose?

A

Lubrication and binding of bolus for swallowing.
Antibacterial, digestive and solvent, evaporative cooling (panting).
Contains 98-99.5% water, mucin, amylase, bicarb, lysozyme and antibodies, urea (ruminants).

96
Q

How is saliva formed?

A
  1. Acini secrete fluid (contains protein, mucin and electrolytes in similar conc to plasma).
  2. Passes through ducts, ionic composition modified. Rate of flow affects composition.
  3. Na and Cl reabsorbed and K and HCO3 secreted still in ducts.
  4. Final product released. Hypotonic (lower osmolarity than ECF).
97
Q

Is saliva hypotonic?

A

Yes.

Osmolarity increases as flow rate increases.

98
Q

Is ruminants saliva hypotonic?

A

No - isotonic with plasma.

Continues buffering to decrease acid build up in rumen.

99
Q

What is the major hormone influencing the composition of saliva?

A

Aldosterone

Controls Na reabsorption in ducts.

100
Q

How is saliva production and secretion neurally regulated?

A

Autonomic NS
PNS - vagal and glossopharyngeal n. Anticipation, chewing and taste bud stimulation all initiate response. Increased blood flow increases volume and water consistency rich in enzymes, predominates during meals.
SNS - secretory cells contain beta-adrenergic receptors. Activated by sympathetic nerves of circulating catecholamines. Increased amylase, constriction of blood vessels supplying glands, decreased saliva, more viscous.

101
Q

How does the SNS affect saliva production in cats?

A

Increases salivation.

102
Q

What is the clinical significance of saliva?

A

Xerostomia - dry mouth - drug relates, insufficient blood flow, radiation, autoimmune disease.
Drooling - excess salivation, remove sublingual glands.
Blockage of oesophagus - dehydration and acidotic ruminants.

103
Q

What are the functions of the stomach?

A 
Short term storage reservoir.
Secretion of intrinsic factor.
Chemical and enzymatic digestion is initiated, particularly of proteins.
Liquefaction of food.
Slowly released into SI.
104
Q

Which cell types and are responsible for gastric secretions and where are they located?

A

Gastric Glands - mucous neck cells (mucous), peptic/chief cells (pepsinogen, renin), parietal cells (HCl, intrinsic factor).
Pyloric gland - G cells (gastrin), mucous neck cells (mucous).

105
Q

What is the function of mucous secretion in the stomach?

A

Protection.
Contains glycoproteins.
Barrier against micro-organisms and endotoxins.
Lubricates mucosa.
Secretion stimulated by cholinergic vagal fibres.

106
Q

How is pepsinogen converted to pepsin?

A

Stored as zymogen in chief cells.
Converted by HCl.
Optimum activity at pH2, inactivated by neutral pH in duodenum.
Secretion stimulated by cholinergic vagal fibres, histamine and gastrin.

107
Q

What is rennin?

A

Chymosin
Proteolytic enzyme - causes milk to curdle in stomach, allows its retention and slow release.
Rennin secretion is highest in first few days post birth, replaced by pepsin as major protease.
Secreted in inactive form (prochymosin), activated by exposure to acid.

108
Q

What does intrinsic factor bind to?

A

Vitamin B12 in the duodenum.

109
Q

Describe the formation of gastric acid (HCl)?

A

Secreted by oxyntic/parietal cells.
H and Cl ions actively transported by seperate pumps.
H within cell derived from carbonic anhydrase (break down of CO2 and H20).
1) K is transported into the cell, pushing H out (into lumen) via breakdown of ATP (H/K/ATPase pump in canaliculi membrane).
2) K diffuses via ion channel back out.
3) Cl/HCO exchanger brings Cl into cell and HCO out into blood.
4) Cl pumped out of the cell via ion channel (into lumen).

110
Q

How is acid secretion within the stomach regulated?

A

Stimulated by; gastrin, histamine, ACh.

Inhibited by; presence of digesta in duodenum, low pH, CCK and secretin, ENS.

111
Q

What are the 3 phases of gastric acid secretion?

A

Cephalic - vagus influences.
Gastric - local nervous secretory reflexes, vagal reflexes and gastrin-histamine stimulation.
Intestinal - nervous mechanisms, hormonal mechanisms.

112
Q

What other mechanisms does the stomach use to reduce secretion?

A

Emptying - decreased protein within stomach decreases secretion.
Somatostatin - decreased food causes accumulation of acids, somatostatin is released which inhibits acid secretion.
Inhibitory component of intestinal phase of gastric secretion.

113
Q

What is the pancreas?

A

Mixed endo- and exocrine gland.
Endocrine portion is islets of langerhans.
Exocrine portion is duct cells (NaHCO3) and acinar cells (digestive enzymes).

114
Q

What is the function of the Islets of Langerhans?

A

Secrete insulin and glucagon.

115
Q

Do the exocrine and endocrine portions of the pancreas have anything in common?

A

No other than location.

116
Q

How is the exocrine pancreas regulated?

A

Hormonally - secretion and CCK.

117
Q

What is a zymogen?

A

Inactive enzyme

118
Q

What are the different pancreatic enzymes?

A

Proteolytic - trypsin (ogen), chymotrypsin (ogen), (pro) elastase, (pro) carboxypeptidase.
Secreted in inactive forms and activated by enzymes.
Amylolytic - amylase (alpha).
Lipolytic - lipase, (pro) phospholipase, carboxyl esterase lipase.
Nucleases - DNAase, RNAase.
Others - (pro) colipase, trypsin inhibitor.

119
Q

What does the exocrine pancreas secreted?

A

Pancreatic juice that empties to duodenum.

2 components - enzymes from acini and aqueous alkaline secretion (HCO3) from duct cells.

120
Q

How are pancreatic zymogens activated?

A

Occurs in luminal border of duodenum.

Enterokinase and trypsin (already present) help convert enzymes to active forms.

121
Q

What does amylase do?

A

Digests starch.
Secreted in active form.
Complete hydrolysis of monosaccharides performed by brush border enzymes.

122
Q

What does lipase do?

A

Fat digestion (also requires bile salts).
Allows formation of water-soluble micelles.
Secretion is stimulated by diets high in fat or protein.
Secreted in active form.

123
Q

What does bicarbonate secreted from pancreas do?

A

Neutralises acid entering duodenum.
HCO3 increases, Cl decreases.
Secreted mainly by epithelial cells of ducts and ductules that lead from acini.

124
Q

What other ions does pancreatic fluid contain?

A

Water
Na
K

125
Q

What is the clinical significance of pancreatic secretions?

A

Decreased enzyme production known as pancreatitis.

Steatorrhea - presence of undigested fat in faeces.

126
Q

What is pancreatic duct secretion mainly governed by?

A

HCO3/Cl exchanger

127
Q

Describe the neural and hormonal regulation of pancreatic secretion.

A

Neural - ACh (extrinsic, ductule and acinus), VIP (intrinsic, acinus), GRP (neutral, acinus).
Humoral - Secretin (ductule), CCK (acinus).

128
Q

What are the phases of pancreatic secretion?

A

Cephalic - vagal cholinergic fibres simulate acinar M3 receptors, enzyme secretion initiated but with only small amounts of H20 and electrolytes secreted with enzymes. Minimal flow through ducts.
Gastric - same as cephalic.
Intestinal - chyme enters small intestine, secretin released due to increased acidity (requires cholinergic input), CCK released in response to fat in lumen (mediates acinar enzyme secretion).

129
Q

What are the functions of the liver?

A 
Secretion of bile.
Metabolic processing of nutrients.
Removal of aged RBC's.
Elimination of wastes from body.
Synthesis of plasma proteins.
Secretion of glycogen, fat, iron, copper and vitamins.
Gluconeogenesis.
Activation of vitamin D.
130
Q

How is the liver arranged?

A

Into hexagonal lobules (sheets of 6 sided hepatocytes).
Hepatocytes bathed by blood from sinusoids (capillary networks with mix of arterial and venous blood) on two sides.
Between each row of cells are cannaliculi into which bile flows.

131
Q

What are Kupffer cells?

A

Liver phagocytes that line the sinusoids and engulf and destroy old RBC’s and bacteria.

132
Q

Describe the liver blood flow.

A

Each hepatocyte in direct contact with venous blood (from GIT) and arterial blood (aorta).
Venous blood enters via hepatic portal system.
Pressure in portal system usually low (10mmHg).

133
Q

Describe the flow of bile in the liver.

A

Secreted from hepatocytes into canaliculi.

Bile duct epithelium can alter its composition (water and electrolytes).

134
Q

What is bile acid composed of?

A

90% of organic portion of bile.
Cholesterol, phospholipids, bile acids, bilirubin.
Combined hydrophilic and hydrophobic sides.

135
Q

What is the main bile acid?

A

Cholic acid.

136
Q

What enables bile acids to exist as bile salts?

A

Conjugation with either taurine or glycine.

137
Q

Are bile salts fat soluble?

A

No - they tend to remain in lumen of SI carrying out emulsification (breaks large fat droplets into small droplets).

138
Q

What is the function of micelles?

A

Transport of water insoluble substances through water.

139
Q

What happens to bile salts post digestion?

A

95% recycled to liver via portal circulation (enterohepatic circulation).

140
Q

What is bilirubin?

A

Product of haemoprotein breakdown.
Fe recycled and pigment processed by liver. Following its excretion in bile, conjugated bilirubin is reduced by intestinal bacteria to form urobilinogen. This is either absorbed by SI or oxidised to stercobilin (brown colour of stool).

141
Q

What is the clinical significance of bilirubin?

A

Excessive haemolysis or blockage of bile duct causes increase of plasma bilirubin. Causes Jaundice.

142
Q

Where does non-fermentative digestion occur?

A

Stomach, abomasum and SI.

143
Q

What is the physical breakdown of food and why is it important?

A

Mastication, grinding of distal stomach.

Important for reduction of particle size and enlarging surface area.

144
Q

What is chemical digestion of food?

A

Reduction of complex nutrients into simple ones.

Accomplished via hydrolysis.

145
Q

What are the 2 classes of digestive enzymes?

A

Act within lumen of gut (Luminal phase of digestion) - originate from glands, mixes with digesta, causes incomplete hydrolysis of nutrients.
Act at membrane surface of epithelium (membranous phase of digestion) - chemically bound, break short-chain polymers to monomers.

146
Q

Describe membranous phase digestion.

A

Comprises of unstirred water layer, mucous and glycocalyx. Enzymes project from apical membrane into surface layer.
Peptides and polysaccharides diffuse here from lumen, broken down and then absorbed.

147
Q

What are the stages of CHO digestion and absorption?

A
  1. Dietary polysaccharides, starch and glycogen convert to maltose by salivary and pancreatic amylase (luminal phase).
  2. Small sugars (maltose, lactose) converted to monosaccharides by brush border enzymes (membranous phase).
  3. Glucose and galactose absorbed across apical membrane by cotransport with Na (mem. phase).
  4. Fructose absorbed by facilitated diffusion (mem. phase).
148
Q

What are the stages of protein digestion and absorption?

A
  1. Dietary and endogenous proteins hydrolysed by gastric pepsin and pancreatic proteolytic enzymes.
  2. AA absorbed across apical membrane via cotransport with Na.
  3. Small peptides absorbed by different carrier - broken down to AA by brush border enzymes.
149
Q

Describe the digestion and absorption of fats?

A

Detergent action needed to emulsify/dissolve.
Pattern of digestion similar to CHO and proteins - large molecules undergo enzymatic breakdown (lipase) into smaller molecules.
Absorption of lipid soluble vitamins occurs along side.
Occurs mostly in SI via pancreatic lipase - needs to undergo emulsification by bile salts before they can be digested by water soluble lipase.

150
Q

How much fat can ruminants tolerate in their diet?

A

8%

151
Q

What are the primary dietary lipids?

A

Triglycerides
Phospholipids
Cholesterol

152
Q

What are the 4 phases of lipid assimilation?

A
  1. Emulsification (bile salts - makes it water soluble).
  2. Hydrolysis (lipase)
  3. Micelle formation
  4. Absorption
153
Q

What are the stages of lipid digestion and absorption?

A
  1. Emulsification via bile salts, increases SA.
  2. Lipase hydrolyses triglycerides into monoglycerides and FFA.
  3. Monoglycerides and FFA carried in interior of water soluble micelles.
  4. Near absorptive epithelial surface the monoglycerides and FFA leave micelle and passively diffuse through lipid bilayer.
  5. Resynthesised into triglycerides in epithelial cells.
  6. Triglycerides aggregate coated with lipoprotein layer. Water soluble chylomicrons are extruded by exocytosis.
  7. Chylomicrons enter lymph vessels because they can’t enter capillaries.
154
Q

What is the main primary active transport pump?

A

Na/K pump

155
Q

What are the forms of secondary active transport?

A

Cotransport

Countertransport

156
Q

What are the forms of tertiary active transport?

A

Driven by electrochemical gradients established by secondary transport.
Cl/HCO3

157
Q

Which two ways can passive transport move through substance?

A

Transcellular - movement though cell.

Paracellular - movement through tight junctions.

158
Q

What are the 3 mechanisms of Na absorption?

A
  1. Na cotransport (with glucose, galactose, AA, bile salts)
  2. Na/H exchanger - coupled with Cl/HCO3 exchanger.
  3. Diffusion of Na down concentration gradient through ion channels in apical membrane.
159
Q

What are the 3 mechanisms of chloride absorption?

A
  1. Coupled Na/Cl absorption (Na/H, Cl/HCO3).
  2. Paracellular Cl absorption - cotransport with Na.
  3. Cl/HCO3 exchanger without coupled Na absorption.
160
Q

Is bicarbonate reabsorbed?

A

Yes - in distal ileum and colon via Na/H exchange mechanism.

161
Q

Where is water absorbed in the GIT?

A 
Upper SI mucousa freely permeable to water. 
Paracellular absorption (via diffusion).
162
Q

In what direction will water move in the intestine?

A

Moves in whichever direction is necessary to keep ingest iso-osmotic

163
Q

What factors influence water absorption?

A

Blood flow to GIT.
Sum of osmotic and hydrostatic forces.
Collective action of various intestinal absorptive mechanisms that concentrates solutes in lateral spaces.
Diffusion gradient

164
Q

What is the action of villous cells?

A

Absorption

165
Q

What is the action of crypt cells?

A

Secretion - uses Cl transport mechanism.

166
Q

What are the stages of Active Cl secretion?

A
  1. Na and Cl enter crypt cell via cotransport on basolateral membrane.
  2. Na pumped out by Na/K pump.
  3. Cl enters lumen through channel (cAMP) on apical membrane.
  4. Negative Cl in lumen attracts Na by paracellular pathway. Water follows.
167
Q

What is diarrhoea?

A

Increase in frequency of defection or increase in volume due to increased water.
Symptom, not a disease - mismatch between secretion and absorption.

168
Q

What are the 5 basic causes of diarrhoea?

A 
Hypersecretory - excess water.
Osmotic - not absorbing sugars/electrolytes.
Exudative
Malabsorptive
Altered motility.
169
Q

What is malabsorptive diarrhoea?

A

Inadequate absorption.
Loss of epithelium and reduction in absorptive area - intestinal damage, villous atrophy, crypt damage, inflammation.
May be viral, bacterial or protozoal.
Decreased SA and mature cells lost - loss of enzymes for membranous phase digestion and transport proteins.

170
Q

What is hypersecretory diarrhoea?

A

Rate of intestinal secretion is greater than absorptive capacity.
Primarily due to inappropriate secretion from SI crypts - abnormal stimulation.
Causes may be viral, enterotoxins or chemical/pharmacological.
Enterotoxins bind to enterocytes, stimulate adenyl cyclase activity and production of cAMP within cells, opens Cl gates and secretes water and electrolytes from crypt epithelium.
E coli.

171
Q

What is osmotic diarrhoea?

A

Lactase deficiency, lactulose, magnesium sulfate (laxative), maldigestive problems.

172
Q

What is exudative diarrhoea?

A

Infectious - salmonella.

Bacterial damage to mucous epithelium, decreased absorption and release of inflammatory proteins.

173
Q

What is altered motility diarrhoea?

A

Reduced transit time (surgery, neural dysfunction).
Bacterial overgrowth.
Various diseases causing GI stasis.

174
Q

What is fermentation?

A

Metabolic action of bacteria and other micro-organisms.

Molecular substrates are broken down.

175
Q

Is enzymatic hydrolysis essential for fermentative digestion?

A

Yes.

176
Q

What differences are their between fermentative and glandular digestion?

A

Fermentative is slower and requires microbes. Also has greater extent of alteration to large molecules.

177
Q

What conditions do microbes require for fermentation?

A

pH close to neutral - 6-7.
Temp 39 degrees.
260-280mosm.
Oxidation reduction potential -250 to 450mv.
Slow rate of flow to allow multiplication.

178
Q

What are the 5 major groups of microbes within rumen, caecum, colon?

A 
Bacteria
Protozoa
Fungi
Archaea (methanogenic)
Bacteriophage
179
Q

Describe how ruminants and microbes have a symbiotic relationship?

A

Microbes provide nutrients to ruminant - digestion of cellulose and hemicellulose.
Provision of high quality protein and B vitamins (particularly cobalt).
Detoxification of toxic compounds.

180
Q

Name some rumen bacteria.

A

Widely adapted - selenomonas, lactobacilli.
Cellulose and hemicellulose - ruminococcus
Starch - streptococcus bovis
Mono-/Disaccharides - lactobacilli
Lactate and simple sugars - selenomonas.

181
Q

Name some methanogens.

A

Methanobacterium ruminantium.

182
Q

Name some protozoa.

A

Holotrich - covered in cilia, utilise starch and soluble sugars. Produce acetic, butyric and lactic acid.
Entodiniomorphid - tufts of cilia.

183
Q

What are the 3 groups of plant CHO digested by ruminants?

A

Insoluble structural polysaccharides - cellulose, hemicellulose.
Soluble structural polysaccharides - pectin, beta glucan.
Storage mon-, oligo-, polysaccarides - starch, fructan, water soluble CHO.

184
Q

How is lignin broken down?

A

Fungi.

Resistant to action of mammalian and microbial enzymes.

185
Q

Which enzyme acts on hemicellulose, cellulose and pectin?

A

Cellulase.

Further metabolised by microbes.

186
Q

Which is the only VFA that can converted to glucose?

A

propionate.

187
Q

What are the end products of CHO digestion?

A

Acetate
Butyrate
Propionate

188
Q

What is the major VFA produced?

A

Acetate.
Then propionate and then butyrate.
Same for both high fibre and high starch diets.

189
Q

Why are VFA’s important?

A

End product of anaerobic microbial metabolism.
Still contain considerable energy which can be derived from aerobic metabolism.
Accumulation of VFA’s suppresses or alters fermentative process by decreasing pH.
Host animal maintains conditions for fermentation by buffering and removing VFA’s via absorption.

190
Q

What are the 2 forms of dietary protein and how are they fermentatively digested?

A
  1. True protein - rumen degradable/microbial or undegradable protein which goes to abomasum.
  2. Non-protein nitrogen (urea, ammonia, nitrate) - microbes use this for body growth and incorporate it into bacterial protein in presence of rich CHO diets.
191
Q

How is microbial growth linked to protein utilisation?

A

Glucose and peptide availability is appropriately matched - energy from glucose, peptides for microbial protein synthesis.
Relationship between two has massive impact on microbes and thus the host.
Glucose + peptides = Microbes + VFA + NH3 + CH4 + CO2

192
Q

What is urea? How is it excreted?

A

Nitrogenous waste product formed in liver - arises from deamination of AA.
Ruminants - excreted into rumen
Monogastric - excreted by kidneys

193
Q

What is biohydrogenation? Where does it occur?

A

Addition of H across double bond to saturate unsaturated FA.

Occurs in rumen when LCFA adhere to feed particles and microbes.

194
Q

What effect does fat have on rumen microbes?

A

Inhibitory action above 5-6% on forage digestibility.
Caused by antimocrobial activity of LCFA liberated by lipolysis in rumen.
Effect overcome by adding calcium hydroxide.
Can also feed protected fat - bypasses rumen microbes and digested in SI.

195
Q

What are the other functions of microbes and fermentation?

A

Synthesis of B vitamins (microbes require these)- B12 requires cobalt to be present.
Defense against dietary toxins.

196
Q

Describe the non-fermentative function of the LI.

A

Absorption of electrolytes and water.
Higher electrochemical gradient due to tighter mucosa.
Absorption of water, Na, Cl, HCO and secretion of K.
Ion transport mechanisms similar to SI - active Cl secretion not present though.

197
Q

Describe the equine hindgut.

A

Absorptive and fermentative functions complement each other.
Disturbances in fermentation cause abnormalities.
Major substrates are structural and nonstructural CHO, proteins.
Hindgut fermentation aided by prior gastric action - increased digestion when increased microbial breakdown, some CHO digested and absorbed before hindgut.
Glandular digestion in horse not very efficient.

198
Q

Describe VFA production in equine colon.

A

Large quantities of fluid rich in HCO3 and P buffers secreted by ileum and transferred into caecum.
Addition of bicarb and other electrolytes in colon.
VFA production starts in caecum and continues in colon.
Large fluxes of water enter hindgut from blood via mucosa - due to direct secretion from crypts of colon epithelium.
High concentration of VFA’s in lumen - increased Na, HCO and Cl fluid secreted.
Molecular mechanisms of VFA absorption appear identical to ruminant.
Absorption of VFA and Na causes absorption of water.

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