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GI Physiology > GI > Flashcards

GI Flashcards

1
Q

List the overall function of the digestive system

A
  1. replace water lost by renal and respiratory systems
  2. replace electrolyes lost by renal system (Na, Cl, Ca, Mg)
  3. replace cellular building blocks (amino acids, lipids)
  4. Replace vitamins
  5. energy (CHO, AA, Fat)
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2
Q

What must the digestive system do to obtain its functions?

A

motility
secretion
digestion
absorption

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3
Q

What is required for motility and what does it do?

A

requires smooth muscle contractions.

mixes food with saliva and digestive enzymes, mechanical break down, move food through the GI

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4
Q

Where is skeletal muscle located in the GI and why is it important?

A

location: mouth, anus, esophagus
importance: voluntary control and innervation
NOTE: smooth muscle has a constant level of muscle tone

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5
Q

What time of secretions occur in the GIT?

A

Exocrine glands (water, electrolytes, mucous chemicals, enzymes)
- secretory cells transport raw material from blood into themselves, assemble material and secrete into lumen
- releases when neural or hormonal stimulation
- contents are often recycled
Endocrine (local chemical mediators)
- common in GI (short term and long term)
- paracrine (between cells)

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6
Q

Basic components of food?

A

Carbs, Fat, Protein

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7
Q

What is a monosaccharide?

A

glucose, fructose, galactose

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8
Q

What is a disaccharide?

A

lactose (glucose + galactose), sucrose (glucose + fructose), maltose (2 glucose)

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9
Q

Carbohydrate enzymes?

A

amylase, maltase, sucrase, lactase

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10
Q

what is a polysaccharide?

A

starch (glucose alpha 1,4)
cellulose (glucose beta 1,4)
hemicellulose (xylose beta 1,4)

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11
Q

What is required for mammals to digest cellulose and hemicellulose?

A

Fermentation by microbes containing enzymes

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12
Q

Generally, how is protein broken down?

A

protein > polypeptides > small peptides & aas

enzymes: trypsin, chymotrypsin, carboxypeptidase, pepsin, aminopeptidase, HCl

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13
Q

Generally, how is fat broken down?

A

Triglycerides = glycerol + 3 fatty acids
absorbable: monoglycerides + fatty acids
Enzymes: lipase, esterase

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14
Q

what is the general process of absorption? (layers is crosses)

A

Apical side > basolateral side > circulation

CHO and protein (transporters are required)

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15
Q

where does absorption occur and what is absorbed?

A

Stomach: little
SI: nutrients, most electrolytes, water
LI: water, some electrolytes

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16
Q

Compare and contrast carnivores, herbivores and omnivores?

A

Carnivores: energy dense, low carb high protein and fat, simplest
Omnivores: flexible, more complex
Herbivores: low fat, moderate protein, low energy, require fermentation, most complex and longest

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17
Q

Compare and contrast pre-gastric and post gastric fermentation?

A

pre: before glandular stomach, microbes
e.g. ruminants, pseudoruminants (camelids, 3 chambers), (Marsupials, hippo, sloths - outpouching before stomach)
Post: microbes after stomach
large cecum - lagomorphs, rodents (capibara, worlds largest)
large colonic fermenters - equidae, rhinos, elaphants

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18
Q

Name the 4 tissue layers

A

Mucosa, Submucosa, Muscularis externa, serosa

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19
Q

what are the 3 layers within the mucosa?

A 
folded layer containing:
Mucosa membrane (epithelial cells)
Lamina propria (CT, vessels and lymph, nerves, immune)
Muscularis Mucosa (thin later of smooth muscle
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20
Q

characteristic of the submucosa?

A

thick CT later
larger lymph and blood
neurons: submucosal nerve plexus (enteric nervous system)

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21
Q

Two layers within the muscularis externa?

A

outer longtitudinal and inner circular

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22
Q

characteristics of the serosa?

A

outer CT attached to mesentery

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23
Q

Name 3 types of cellular connections in the GIT?

A
  1. occludens “6-pack rings”
    - tight junctions on apical portion
    - transcellular transport (through the cell)
  2. Adherens
    - attached by proteinacous material
    - paracellular transport (between cells)
  3. Gap junctions
    - propagation of action potential throughout smooth muscle
    - sm m syncytial contractions
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24
Q

What is the general term for blood supply to GIT (stomach, intestine, colon, cecum, spleen, pancrease, liver)

A

Splanchnic circulation

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25
Q

What artery supplies stomach, proximal duodenum, spleen and liver?

A

Celiac -> gastric, hepatic, splenic

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26
Q

What artery supplies most of SI, cecum and colon?

A

Cranial and Caudal Mesenteric

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27
Q

Explain venous drainage from the abdominal cavity

A

GI venules > veins > portal vein > liver > hepatic vein > caudal vena cava
Point: all blood goes through the liver

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28
Q

Why is portal circulation important for xenobiotic metabolism?

A

Liver receives absorbed nutrients and toxins before any other tissue
hepatocytes metabolize the toxins and drugs before going to the heart

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29
Q

What is portal circulation important for nutrient metabolism?

A

Liver receives absorbed nutrients first

storage system for sugars and triglycerides

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30
Q

What is the purpose of anastomoses in GIT?

A

NOTE (arterioles penetrate muscularis externa, submucosa
capillaries: many crpyts an villi)
These connections allow for damages and lack of perfusion to be compensated for. Occluded areas can be bypassed.
Parallel rather than series circuits.

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31
Q

The intestinal villus has counter current flow, what does this allow it to do?

A
  1. creates oxygen gradient
    - higher at base, lower at tip
    - enhance mucosal shedding at surface
  2. Hemorrhage
    - blood is shunted away from tip during hypovolemia
    - if intensified can get villus ischemia = necrosis
  3. hyperosmotic lumen and water loss
    - during luminal osmotic pressure water can be drawn from circulaiton
    - blood can be shunted away to minimize fluid contact
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32
Q

Why does perfusion increase during the fed state?

A

increase activity
provide oxygen and nutrients to facilitate motility, secretion and absorption
NOTE: blood flow increases due to increase GI function (not other way)

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33
Q

what causes increased GI blood flow (perfusion)?

A

GI hormone release (CCK, Gastrin, Secretin)
Enteric neurotransmitters
- Ach (binds to muscarinic and nicotinic receptors in parasym)
- vasoactive intestinal peptide (VIP)
- NO
- serotonin
- prostaglandins

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34
Q

How do NSAIDS affect blood flow to GI?

A

NSAIDS block prostaglandins causing hyper-perfusion that can damage epithelial mucosal cells

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35
Q

What will happen to GI blood flow during exercise/ hemorrhage/acute stress/fasting?

A

Increased sympathetic firing decreases parasympathetic = decreased GI flow
GI vasoconstrictors: nor-epi (alpha 1 adrenergic receptors)(endocrine or from splanchnic nerve NT)
neuropeptide YY

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36
Q

Explain autonomous smooth muscle contractions?

A
  • do not have constant membrane potential (will slowly depolarize and depolarize)
  • “baseline” resting membrane potential will change
  • similar to cardiac pacemaker (except doesn’t reach potential all the time)
  • can function independent of CNS
  • coordinated response
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37
Q

What comprises the enteric nervous system (intrinsic) ?

A

Intrinsic nerve plexuses : myenteric and submucosal nerve plexuses
Afferent neurons:
- mechanical receptors in muscularis mucosa (pressure)
- mechanical receptors in muscularis externa (tension/tone)
- chemoreceptors and osmoreceptors detect pH and osmplarity in lumen
Efferent:
- relay signals to effectors cells
- synapse with smooth muscle (stimulate/inhibit)
- synapse with glands (induce secretion of exocrine glands into lumen; and endocrine hormones)
Interneurons: “bulk of neurons” “coordination”
- take incoming info from afferent fibres and regulate stimulation to efferent fibers > effector cells

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38
Q

What are some excitatory NTs of the ENS? What do they do?

A

produce slight depolarization of post synaptic cell.

e.g. Ach, Serotinin (many receptors) or substance P (pain signals)

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39
Q

What are some inhibitory NTs of the ENS? What do they do?

A

postsynaptic hyperpolarization through ion channel activation or inhibition

  • increase K influx
  • increase Cl- influx
  • decrease Ca influx

what are they?
NANC (non-adrenergic-cholinergic inhibition)
e.g. vasactive intestinal peptide (cAMP, cGMP)
- opioids/enkephalins
- somatostatin

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40
Q

What is the Extrinsic nerve system and what nerves predominate?

A

Autonomic system (para and sympathetic)

afferent nerves > efferent (same as ENS

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41
Q

Explain how sympathetic neural activity will affect GIT?

A

decrease GI motility
Pre-ganglionic: ACh -> Nicotic
Post- ganglionic: Nor-epi -> alpha1 adrenergic receptors

sympathetic inhibits the cholinergic excitatory branches

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42
Q

Explain how parasympathetic neural activity will affect GIT?

A

increase GI motility, secretion and blood flow.
Primary: vagal nerve (pancreas, gall bladder, distal esophagus, stomach, SI and prox colon)
pelvic nerve (distal colon)

Ach –> nicotinc (enteric nerve plexi) & muscarinic receptors (smooth muscle)

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43
Q

Whats the point of extrinsic if you already have ENS? give para and sym examples.

A

with the CNS in the extrinsic you can incoorperate larger GI motility and secretions

E.g. Parasympathetic extrinsic control
Cephalic phase: smell of food stimulates gastric motility and secretion
Parasympathetic is bringing together what you are sensing and priming the GI tract with anticipation of what’s coming
Enteric cant do this until the food is actually there.

e.g. Sympathetic
Ileus: complete inhibition of GI motility due to:
Mechanical cause (obstruction, impaction_
Surgery, peritonitis, pain
E.g. hardware disease in cattle, colicky horse or calf, animals post surgery

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44
Q

Whats the purpose of endocrine function in the GIT? how does it work?

A

Enteroendocrine cells release gastrin, secretin and cholecystokinin etc.

helps further coordinate the functions of the GIT

e.g. Gastroileal and Gastrocolic reflexes (gasttrin secreted into the stomach and into the blood, blood stream helps stimulate motiltiy further down)

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45
Q

what is the purpose of local paracrine control int he GIT? Examples?

A
  • can act as NTs and paracrine mediators

Prostaglandin

  • help maintain vascular flow
  • stimulate mucosal protection

Cytokines

  • IGF (insulin like growth factor)
  • EGF (epidermal like growth factor)
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46
Q

What are the 3 contributers to GI function?

A

ENS, Extrinsic autonomic nerves, GI hormones.

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47
Q

Characteristics of smooth muscle?

A

actin and myosin loosely arranged so no striations

  • no troponin
  • actin and myosin bind if myosin is phosphorylated
  • relies on extracellular Ca+
  • longer latent period (takaes longer for Ca to enter smooth muscle cytoplasm)
  • relaxation is slower because it must pump Ca out via CaATPase pump
  • less energy required
  • doesn’t fatigue
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48
Q

What problems can you see with smooth muscle relying on extracellular plasma?

A

extracellular fluid equilibrium with plasma. Hypocalcemia smooth muscle will be impacted before skeletal.
e.g. milk fever

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49
Q

Explain the contraction process once Ca is released?

A
  • Ca binds to calmodulin
  • calmodulin activates myosin light chain kinase
  • MLCK phosphorylates myosin
  • myosin binds to actin (cross bridge)
    = contraction
  • myosin light chain phosphatase removes phosphate
  • ATP must separate proteins
  • Ca must be pumped out (CaATPase)
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50
Q

What is the significant characteristic of visceral smooth muscle in the GIT?

A

Fibers act together as one unit
- excitatory signals conducted via gap junctions from cell to cell

different from multi-unit smooth muscle in vasculature

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51
Q

What are the specialized pacemaker cells in the GI? what do they do?

A
  • spontaneous activity (slowly depolarize and repolarize)
  • lie between circular and longitudinal sm m
  • when threshold is reached = multiple spikes
  • electrical activity is passed through gap junctions to muscle cells
  • more slow wave frequency in proximal intestine pacemaker cells
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52
Q

What what influences slow wave potentials?

A

hitting threshold isnt always reaches
- depends on resting potential and amplitude of slow wave potential

  • parasym AcH increases resting and amplitude
  • VIP released by ENS will hyperpolarize
  • presence of food will increase potential proximal to food bolus
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53
Q

how does SMm contraction propel food?

A

distal to bolus: circular inhibition and longitudinal stimulation
Proximal to bolus: circular muscle stim and longitudinal inhibition

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54
Q

What is stress-relaxation? how does it happen?

A

food enters: sudden stretch triggers initial tesnion, followed by return to resting tension

active cross bridge formation occuring followed by loss of attachement

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55
Q

What is reverse stress-relaxation?

A

Food leaves: sudden decrease in tension, followed by build up up tension to resting level

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56
Q

In combination what does stress-relaxation and reverse stretch relaxation accomplish in the GIT?

A

allows tube to keep relatively constant tone during food passage and changes in luminal distension

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57
Q

Whats the purpose of mastication?

A

mechanical break down
mix with saliva
trigger GI secretions

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58
Q

What muscles are used in mastication?

A 
Massseter, temporalis (CN V)
Linguinal muscles (CN VII)
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59
Q

How do carnivores drink?

A

Dogs - ladle

Cats - surface tension (no bristles on tip)

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60
Q

What substances do saliva secreting cell produce?

A

serous cells - water and electrolytes
mucous cells - viscous glycoprotein rich
duct cells - reabsorb Na, Cl; secretes K+ and bicarb

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61
Q

What glands secrete saliva?

A

Parotid (watery) - herbivores
submandibular (mucous and serous)
sublingual (mucous)
Minor glands: buccal, lingual, palatine

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62
Q

What does saliva do?

A 
Digestion - amylase (questionable), Lipase (medium chain fatty acids in neonatal milk, important b/c less pancreatic enzymes), proteases (some rodents)
lubrication
anitbacterial
vocalization
heat loss in panters
neutralize acids
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63
Q

How are the ingredients transported into the acinar cells from the plasma for saliva secretion?

A

ion channels and aquaporins and Na+/K+ ATPase creates a concentration gradient.

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64
Q

Why does saliva composition depend on flow rate?

A

if the flow rate increases cells dont have enough time to reabsorb

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65
Q

What can change saliva production in cattle?

A

more roughage diet more stimulation and saliva production

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66
Q

What regulates saliva production?

A

CN IX - paratid gland
CN VII - submadibular, sublingual

stimulates by parasympathetic (AcH/Musc) = myoepithelial contraction

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67
Q

What drugs cause dry mouth?

A

atropine (anticholinergic drug)

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68
Q

How does sympathetic stimulation affect saliva?

A

more mucous and protein (viscous and dry)

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69
Q

Explain unconditioned and condition salivary reflexes.

A

unconditioned - chemoreceptors and pressure receptors in the mouth are stimulated
conditioned - pavlovs dogs

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70
Q

what does aldosterone do to saliva production?

A

increases Na reabsorption in salivary ducts, more Na/K ATPase activity (same as kidney)

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71
Q

whats significant about absorption in the mouth?

A

bypasses the liver (drugs)

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72
Q

What are 3 salivary pathologies?

A

Sialocele - subcutaneous cavity in the face containing saliva (trauma, obstruction, infection)
Sialolithiasis - mineralization
Xerostomia - dry mouth syndrome (chronic meds)

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73
Q

explain the reflex arc of swallowing?

A

voluntary first then involunatary

afferent nerves > swallowing center (medulla) > efferent nerves > muscles

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74
Q

Explain the process of the oropharyngeal phase of deglutition (swallowing)?

A
  • pressure receptors in pharynx
  • tongue traps food against hard palate
  • uvula prevents into nasopharynx and epiglottis prevents into trachea
  • swallowing centre inhibits resp centre (don’t breathe at same time)
  • striated pharyngeal muscles contract propels food down
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75
Q

what are the functions of the two esophageal sphincters?

A

pharyngo-esophageal: prevents air from entering esophagus (more of a band)
gastroesophageal: prevent acid from coming back up (higher tone)

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76
Q

What is the function of the pharyngeal esophageal sphincter during swallowing?

A

increase in pharyngeal pressure due to muscle contraction opens sphincter, it increases in pressure after to prevent regurgitation.

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77
Q

Explain peristalsis or esophageal phase of swallowing?

A
  • contraction of circular smooth muscle pushes food forward
  • mostly striated muscle (glossopharyngeal IX and vagal nerve X fibres)
  • gastroespohageal sphincter opens upon pressure stim
  • not gravity dependent
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78
Q

What occurs physiologically when food is stuck?

A
  • stimulates pressure receptors
  • local ENS response
  • second powerful peristaltic wave
  • increase saliva production
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79
Q

What causes heartburn?

A

Heartburn - failure of gastroesophageal sphincter to close. Therapy = deal with acid (proton pump inhibitors and antacids)

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80
Q

What caused the star-gazing dog in the case study?

A 
endoscopy found lesions on gastroesophagela spincter
by lifting head, minimizing acid reflux
started sucralfate (coats) ; famotidine (H2 receptor blocker) ; omeprazole (proton pump inhibitor)
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81
Q

What is Dysphagia?

A

difficulty swallowing in oral, pharyngeal or esophageal phase
oral: swelling, neuro (XII or V), ulcers
Pharyngeal: XI or X, muscle dysfunction, aspirational pneumonia

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82
Q

What is Achalasia?

A

during swallowing GES increases in tone, accumulation in distal esophagus

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83
Q

What is megaesophagus?

A

congenital
neurological or myogenic cause associated with endocrine deficiencies.
regurgitation.
Treatmen: cholinergic drugs and steroids, dietary modulation (chair eating)

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84
Q

What comprises gastric mixing?

A

smooth muscle pacemaker cells in upper fundus are autonomous

  • if they reach threshold = wave of smooth muscle will occur
  • strongest in antrum (thick muscle)
  • pushes towards pylorus
  • when it hits sphincter it closes and retropulsion occurs (mixes with HCl and enzymes, mechanical digestion)
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85
Q

Explain gastric emptying?

A

pyloric sphincter is normally open slightly to allow some chyme through
- amount of food passing through depends on how liquidy it is

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86
Q

What are three main controllers of gastric emptying?

A
  1. distension of stomach (increase)
  2. food material in duodenum (decrease) (enterogastric reflex)
    - Fat
    - acid
    - hypertonicity (glucose and aa in duodenum)
    - distension
  3. CNS autonomic nerve reflexes (hunger pains)
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87
Q

Explain the pre-vomiting phase of emesis?

A

movement of chyme form proximal duodenum back to stomach and esophagus (reverse peristalsis)

  • retching or dry heaves
  • salivate, pace, vocalize
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88
Q

Explain the vomiting phase of emesis?

A

no reverse peristalsis but

coordinated skeletal muscle contractions and upper GI relaxation

89
Q

Anatomically/physiologically, what assist the chyme in exiting the oral cavity?

A
  • deep inspiration against glottis
  • all sphincters relaxed
  • contraction of diaphragm and abdominal muscles
  • glottis is closed (closes trachea) uvula covers nasopharynx
90
Q

Compare and contrast regurgitation and vomiting.

A

Vomiting:
expulsion of partially digested food from stomach or intestine and requires skeletal muscle (prodromal signs in animal)
Regurgitation:
expulsion of undigested food from esophagus or pharynx
reverse peristalsis, no abdominal contractions

91
Q

What controls emesis?

A

Emetic centre in the medulla will initiate vomiting.

92
Q

What can trigger the emetic centre?

A

Cerebral cortex (prain, sight, taste)
Vestibular (motion)
anticholinergics
chemoreceptors (apomorphine, toxins, drugs, uremia, metaclopramide)
Viscera (pain, distension, drugs (xylazine)

93
Q

Why cant horses/rabbits/rodents vomit?

what species vomit more?

A

increased gatroesophageal sphincter tone
acute angle of esophagus entry

carnivores and pigs

94
Q

What are the consequences of vomiting?

A

loss of fluid
loss of HCl (metabolic alkalosis)
- if bicarb from duodenum is also lost can balance.

95
Q

Compare the different glands in the cardiac fundic and pyloric regions of the stomach.

A

cardiac: short glands (mucous)

Fundic: deeper
mucous neck cells = viscous alkaline mucous
parietal cells = HCl
Chief cells = pepsinogen
enterochromaffin-like cells = histamine

Pyloric: alkaline mucous
G (enteroendocrine) = gastrin
D (enteroendocrine) = somatostatin

96
Q

What is gastric cell turn over? Why does it happen? what are the consequences?

A

gastric neck neck cells rapidly divide (move up to become chief/parietal)

  • occurs every ~3 days
  • occurs due to chemical damage
  • ulcers occur if acid gets to mucosal layer
  • targeted by chemotherapy drugs
97
Q

What is the function of HCl in the stomach?

A
  • activates pepsinogen
  • denatures proteins
  • kills food bacteria
98
Q

How is HCl produced and secreted in the stomach?

A

in parietal cell (H+/K+ ATPase)

  • H+ from dissociation of water and pumped into lumen for K+ in
  • parietal cells need lots of mitochondria
  • OH- left from water forms bicarb
  • bicarb pumped into plasma Cl in
  • Cl diffuses into lumen and forms HCl
99
Q

How is pepsin secreted and what is its function?

A
  • pepsinogen stored in zymogen granules
  • pepsinogen once in lumen can be activated by pepsin or HCl
  • proteins > peptides (at specific linkages)
  • optimal pH is 1.8 - 3.5
100
Q

Why doesn’t our body secrete active pepsin?

A

Would digest your own cell protein without food present

101
Q

Whats the purpose of mucous secretion in the stomach?

A

gastric neck cells at top of pit secrete

  • providing physical defence against acid (bicarb also secreted with mucous)
  • decrease irritation
  • inactivates pepsin
  • vasoactive prostaglandin can stimulate mucous secretion
102
Q

What is the purpose of the intrinsic factor secreted by the stomach? What secretes it?

A

secreted by parietal cells

- binds to dietary vitb12 in SI and facilitates absorption through receptors in the ileum

103
Q

What is significant about chief cells in the the abomasum of calves?

A
  • secrete rennin (not same as RAAS)
  • curdles milk by precipitating Ca caseinate

NOTE: gastric lipase secreted in some other species (little digestive role)

104
Q

What is the purpose of gatrin secretion as a hormone? when is it secreted?

A
  • secreted by G-cells in pyloric region when protein is present
  • stimulates HCl from parietal cells and pepsinogen from chief cells
  • promotes grwoth and regen of mucosal cells
  • increases motility in the stomach, ileum (gastroileal reflex), colon (gastrocolic reflex)
105
Q

What controls gastric secretion in cephalic phase? what is secreted when stimulation occurs?

A

CNS activity

  • chewing, smelling, tasting or thining about food = vagal nerve stimulation to ENS
  • results in HCl pepsinogen and gatrin secretion
106
Q

what controls gastric secretion in the gastric phase?

A

mechanical and chemical stimuli

  • gastric filling = HCl (ENS)
  • protein in gatric lumen = HCl and pepsinogen release (ENS and extrinsic)
  • gastrin release will stimulate HCl and pepsiogen
107
Q

What control gastric secretion in the intestine?

A

pepsin in duodenum stimulates release of intestinal gastrin leads to increased gastric HCl

108
Q

What gastric inhibition factors in the stomach?

A

removal of food
excess drop in pH
- leads to somatostatin from D cells = inhibits parietal cells, G cells, and ECL cells

109
Q

what are some gastric inhibition factors in the intestine?

A
  • fat, acid hypertonicity
    enterogastric reflex (vagal nerve)
    Entergastrones (hormonal inhibition from intestine):
    CCK, secretin, Gastric inhibitory peptide (GIP)(k-cells)
110
Q

what are gastric ulcers?

A

Erosion of mucosal cells allows acid to underact with tissue

if apical surface is disrupted tight junctions are not tight and HCl can get in

111
Q

what is the positive feed back that can occur with ulcers?

A
  • acid and gastrin stimulates histamine from ECL cells

- histamine binds to h2 receptors on parietal cells causing more acid secretion

112
Q

What causes ulcers?

A

Helicobacter pylori
- weakens mucosal layer
NSAIDS
- lower formation of protective prostaglandins in the mucosa
- decrease blood flow and mucous production
chemical that stimulate acid secretion and inhibit ADH release
- alcohol, caffeine, stress

113
Q

what are the consequences of gastric ulcers?

A

colicky sings
profuse bleeding (melena)
perforation of stomach (fatal)

114
Q

What are 4 types of therapies for ulcers? explain how each works?

A 
1. proton pump inhibitors (omeprazole)
long term can be bad because gastrin is up-regulated can cause gastric carcinoids (Cells being over stimulated)
2. H2 receptor blockers (Zantac)
block histamine receptors, reduce acid secretion from parietal cells.
3. antacid
basic compounds (CaCO3, MgCl2, NaHCO3)
4. Misoprostal
PGE2 analogue 
increases mucous production
115
Q

what digestion occurs in the stomach?

A
  • amylase continues (kinda) ineffective at low pH
  • salivary lipase continues especially in neonates and milk
  • MAJOR: HCl pepsin begin protein
116
Q

Does absorption occur in the stomach?

A

no nutrients or water, no transporters, mucous prevent it

alcohol is absorbed in the stomach (slower than intestine)

117
Q

Does eating before drinking keep you from getting drunk?

A

fat in the SI inhibits gastric secretion and motility until duodenum has time to digest the fat
CCK gets released and slows down digestion
alcohol sits in stomach and is absorbed slower

118
Q

What are two types of glands that are found in the pancreas?

A

Endocrine (islets of langerhans) - insulin, glucagon, somatostatin

Exocrine
secretory acinar cells - enzymes
ducts cells - water and sodium bicarb

119
Q

What proteolytic enzymes do the acinar cells contain in pancreas? where are the enzymes stores?

A

stored in zymogogen granules

trysinogen - activated to trypsin by enteropeptidase and trpysin
Chymotrypsinogen - activated to chymotrypsin by trypsin
procarboxypeptidase - activated to carboxypeptidasae by trypsin
proelastase - activated to elastase

120
Q

what do proteolytic enzymes do?

A

hydrolyze different amino acid linkages

121
Q

What carbohydrate enzymes are secreted in pancreas?

A

pancreatic amylase = polysaccharides into disaccharides

122
Q

What lipid enzymes are secreted in pancreas?

A

pancreatic lipase - hydrolyses triglycerides into monoglycerides and 2 fatty acids (primary source in post- neonatal animals)
co-lipase - helps lipase bind to fats

123
Q

what do nuclease enzymes do in pancreas?

A

digest RNA and DNA

124
Q

What is EPI? how does it happen? how can you test for it? Treatment?

A

exocrine pancreatic insufficiency (dogs, cats)
clinical signs: steatorrhea, polyphagia, weight loss
diagnosis: cant diagnose with blood, add pancreatic enzymes to see if it helps.

125
Q

Can pancreatic enzyme composition change over time? why or why not?

A

Exocrine acinar cells are the only cell that makes the enzymes. Little change occurs because it doesnt respons to contents in the gut but just makes what it is programmed to do (not targeted secretion)
super long term can change with gene expression maybe?

126
Q

why does duodenum want to neutralize the HCl coming from the stomach?

A

Less defences, pancreatic enzymes work better at neutral pH, improved microbial function at neutral pH

127
Q

What secretes NaCO3 into duodenum and how does it do this?

A

Pancreatic ducts cells
mirrors the HCl secretion by parietal cells.
carbonic anhydrase = H+ and HCO3
apical side: HCo3 secreted into duct via Cl exhanger, Cl recycled into lumen
Basolateral: H+ secreted into blood (H/K pump)

Na then follows HCO3 to maintain balance

128
Q

In the cephalic, gastric and intestinal phase, what two mechanisms are used to regulate exocrine pancreatic secretion?

A

hormonal or neural signals

129
Q

What regulation occurs in the cephalic phase to regulate exocrine pancreatic secretion?

A
  • the senses will activate efferent vagal stimulation to pancreatic acinar cells
  • cholinergic NTs (Ach)
  • vagal stimulation of gastric G cells (gastrin into blood)
130
Q

What regulation occurs in the gastric phase to regulate exocrine pancreatic secretion?

A

mechanical and chemical signals
vago-vagal response (Ach release) leading to acinar release
- gastrin weakly stimulates secretion (binds to CCK receptor)

131
Q

What regulation occurs in the intestinal phase to regulate exocrine pancreatic secretion?

A

Secretin: released from duodenal mucosal enteroendocrine cells (S-cells)
stimulated when acid is present
carried to blood stream to pancreas where it stimulates NaHCO3 in ducts cells
CCK: released from duodenal mucosal enteroendocrine cells (I-cells)
stimulated with protein and LCFA
binds to pancreatic acinar cells and stimulates vesicle docking, release of stored enzymes
increases transcription/translation long term
Distension of duodenum: vago-vagal response

132
Q

What are 6 non-digestive hepatic functions?

A
  1. nutrient metabolism and storage
    carbs, proteins, fats
  2. toxin metabolism
    detoxify ammonia (urea synthesis)
    phase1: oxidation (decrease toxicity)
    phase2: conjugation (adds a water-soluble moiety, facilitates excretion)
  3. protein formation
    albumin, globulin, fibrinogen, prothrombin
    hormone synthesis: angiotensinogen, thrombopoeitin, IGF1
  4. immune function
    kupffer cells (remove bacteria absorbed by GI)
  5. hemoglobin “recycling”
  6. activation of Vit D
133
Q

Explain the movement of blood through the lobule of the liver and how its different than bile?

A

blood flows from portal vein through sinusoids on lobule to hepatic vein.

bile flows in the opposite direction, small spaces between hepatocytes form canaliculi > bile ductule > bile duct

134
Q

What are kupffer cells?

A

macrophages in sinusoids of the liver, receptor mediated phagocytosis to remove bacteria from intestinal blood, worn out RBCs and recycle hemoglobin

135
Q

How do hepatocytes filter the blood?

A

sinusoids are fenestrated so plasma can wash out and get detoxed by hepatocytes

  • LCFA, bile acids, bilirubin, drugs, dyes
  • transport carriers are used to facilitate thing

detox:
- xenobiotic substances are conjugated (phase1: oxidation (decrease toxicity)
phase2: conjugation (adds a water-soluble moiety, facilitates excretion)), nutrient metabolism occurs and bile is synthesized

bile and other detoxified substances can be secreted into bile canaliculi (efflux pumps!)

136
Q

What is the clinical relevance of these transporters in the liver?

A

When a transporter in the blood is saturated by a drug and another is administered one cant get through and can stick around in the body much longer.

137
Q

How are bile acids recovered from portal blood?

A
  • Na+ dependent carrier mediated transport from plasma by hepatocytes extracts bile acids
  • carrier mediated transport of unconjugated bile acids also occur
  • bile acids are conjugated with glycine (vegetarian) or taurine (carnivores) in cytosol
  • this facilitates movement into the bile duct
138
Q

How is cholesterol metabolism useful in the liver?

A

can be used to synthesize new bile acids

cholesterol –> cholic acid

139
Q

What is the purpose of bile acid synthesis?

A

convert flat, membrane bound lipids into kinked amphipathic, water soluble detergent that can dissolve lipids in aqueous solution

140
Q

What is bile comprised of?

A

water, electrolytes, bile acids, cholesterol, phospholipids, bilirubin, biliverdin.

141
Q

what is choleresis?

A

Bile secretion

142
Q

What are two types of bile acid secretion methods? explain them.

A

Bile acid-dependent: formed because secretion of bile acids from hepatocytes. acids provide osmotic drive for water and electrolytes

Bile acid-independent: little bile acid but bicarb and water are still secreted into canaliculus
- dependent on bicarb (carbonic anhydrase (water and co2 --> bicarb and H+)
- bicarb/Cl- exchange at canaliculus
- paracellular and Cl channel cycling
- Na/H removes H+
- Na/K ATPase required
- Na and water enter canaliculus
(similar to pancreatic duct secretion)
143
Q

What is the primary regulator of bile duct NaCO3 secretion?

A

secretin

acid in duodenum triggers secretin

144
Q

What are 3 categories of gall bladder storage in animals?

A
  1. no gall bladder (horses, rats, some cervids, some birds)
    - continuous flow
  2. concentrating gall bladder (dog, cat, human, poultry)
    - dilute hepatic bile is stored in gall bladder and bile is concentrated by removing water and electrolytes
    - intermittently emptied into duodenum
  3. non-concentrating gall bladder (sheep, cattle, goats, pigs)
    - continuous flow of relatively concentrated bile into gall bladder with further concentration
145
Q

What hormone triggers gall bladder smooth muscle contractions to occur and release bile into duodenum?

A

CCK

146
Q

When is CCK released by the duodenum?

A

Fat and protein in duodenum

147
Q

What are all of CCKs functions?

A
  • inhibits gastric emptying
  • inhibits gastric secretion by inhibiting gastrin (slows digestion)
  • pancreatic acinar cell secretion
  • trigger bile duct secretion
148
Q

What is enterohepatic recirculation? how does it occur?

A

80% of bile salts are reabsorbed in the ileum, 7% in jejunum, 10% in colon (Na+ dependent intestinal bile acid transporters)
NOTE: gut bacteria can deconjugate bile acids making absorbtion less efficient
- taken back (bound to albumin) to hepatocytes via portal vein
- oxidized and reconjugated

149
Q

what does bile acid reabsorption stimulate?

A

release of more bile salts into GI (if fat is present)

release into gallbaldder (if fat is not present)

150
Q

What is the alternative to recycling? What is clinically relevant about the enterohepatic recirculation?

A

production (energetically costly) drugs can be recirculated and last much longer if recycled with bile acids

151
Q

what are bile salts and how do they help with digestion?

A 
Bile salt (amphipathic) = Bile acid + Na/K
detergent activity that breaks down large fatty masses into smaller lipid droplets
- increases SA for lipase
- negatively charged water soluble portion repels others so droplets cant re-coalesce
152
Q

What is oletra and why did it make everyone shit themselves?

A

octoglyceride

  • wasn’t digested by lipase
  • steatorrhea
153
Q

What do bile salts form in combination with lecithin and cholesterol? where is it absorbed?

A

Micelle (so they cant coalesce)

absorbed in SI

154
Q

How do the reticulo-endothelial cells in the liver break down hemoglobin?

A

heme oxygenase opens the heme porphyrin rings = biliverdin

155
Q

why do birds and reptiles have green bile?

A

secrete billiverdin into bile duct

156
Q

Why do mammals have yellow bile?

A

billiverdin reductase converts billiverdin into unconjugated bilirubin and then excreted by diffusing (if not bound to albumin in blood)
- hepatocytes can extract from blood via carrier molecules

157
Q

Why is feces brown?

A

Gut bacteria convert congugated billirubin to stercobillinogen, which is oxidized to stercobillin (brown colour) and excreted

158
Q

why is urine yellow?

A

some billirubin is deconjugated by gut bacteria, and then converted to urobillinogen, this is absorbed by GI tract and become oxidized to urobillin (yellow) and excreted through kidneys

159
Q

What is a common sign of liver damage?

A

elevated liver enzymes in the blood
some can indicate hepatocyte injury
while others can indicate bile back up

160
Q

what are common liver enzymes that are found in the blood?

A

alk Phos, ALT, AST, GGT, SDH

AST can also come from muscle,
Alk Phos from bone

161
Q

What plasma level changes can indicate liver damage?

A 
decreased urea (not being produced from ammonia detox)
increased billirubin (not being extracted from plasma and excreted in bile)
decreased albumin ( liver not producing it)
162
Q

What other diagnostic tests can indicate liver damage?

A

hepatic function test
radiographs
ultrasound

163
Q

What is hepatitis?

A

inflammation of liver cells
acute or chronic
viruses, toxins, bacteria caused
cirrhosis: long term (scar tissue)

164
Q

hypoproteinemia?

A

decreases albumin production with long term liver disease

decreased oncotic pressure in vessles and edema

165
Q

clotting disorders?

A

decreased fibrinogen and prothrombin synthesis

decreased absorption of Vit-K from decreased bile salt production

166
Q

Fatty liver syndrome?

A

fat animals that dont eat or are in negative energy balance
adipose tissue broken down, fat stored in liver
impaired fat digestion
seen in 6/9 7/9 cows and overweight cats

167
Q

Jaundice (icterus)?

A

bilirubin accumulation in the plasma and tissue (sclera, mucosa)

168
Q

What causes Jaundice?

A
  1. hemolysis
    - incresed RBC destruction saturates the livers ability to extract from blood stream into bile
  2. hepatic disease
    - less hepatocytes for bilirubin excretion
    - lowered bile secretion in gut = lower bilirubin excretion (intrahepatic cholestasis = hepatocyte swelling squeezes canaliculi; extrahepatic cholestasis = choleliths (stones))
169
Q

How do you treat neonatal jaundice?

A

put them under blue light

blood transfusions

170
Q

What are bands of muscle around the colon and what does their constriction form?

A

Taeniae coli that form haustra (pouches)

171
Q

What is the digestable and absorbable functions of the LI?

A 
Carnivores/some omnivores
- fluid electrolyte absorption
- minimal fluid absorption
Herbivores/omnivores
- fermentation of cellulose
- fluid and electrolyte absorption
e.g. elephants
172
Q

How do the slow wave contractions in LI compare with stomach and SI?

A

frequency of slow wave potentials is lower than in the stomach and SI

173
Q

Where are two significant pacemakers located in the colon? what do they do?

A

Proximal colon (ileocecal junction)
- infrequent slow wave potentials in an aboral direction
- strong action potential spikes which contraction move towards the rectum
Mid-colon
- slow waves which travel aboral and oral
- weak peristaltic contraction towards cecum

174
Q

What is the purpose of haustral contractions? what controls it?

A
  • nonpropulsive
  • mix fecal material
  • increase absorption and transit time
    Control: autonomous smooth muscle activity initiates contractions
    ENS help control
175
Q

What is the purpose of propulsive contractions? what controls them?

A

peristaltic or reverse peristalsis (more reabsorption)

control: mediated by ENS and autonomic

176
Q

What is the purpose of mass movements? what causes them?

A
  • in species that eat infrequently
    large coordinated contractions of longitudinal smooth muscle of the colon
  • helps move rapidly into distal colon and rectum
    Gastro-colic reflex: food entering stomach will stimulate mass movment in colon (caused by gastrin and parasympathetic nerves (extrinsic)
177
Q

What is the defecation reflex? what stimulates and inhibits it?

A

food material in rectum stimulates stretch receptors in mucosal wall –> casues extrinsic nerve refelx through pelvic nerve

pelvic afferent - signal foes to sacral spinal cord
pelvic efferent - stims smooth muscle in colon and rectum, inhibiting smooth muscle in the internal and external sphicters
sympathetic hypogatric nerve is inhibited
- causes relaxation of internal sphincter

178
Q

What is involved in voluntary control of defecation?

A

external anal sphincter = skeletal muscle
(pudendal nerve)

can prevent defecation: urge will subside (“forgotten”) but will return

179
Q

What is involved in active defecation?

A

strain

  • contracting abdominal muscles
  • force expiration against glottis (valsalva manoeuvre)
180
Q

What is secreted into the lumen of the colon?

A

bicarb - neutralizes SCFA produced by microbes

Mucus - from goblet cells to lubricate and protect

181
Q

Does digestion occur in the colon?

A

no enzymatic digestion (microbial fermentation)
Carnivores - fermenting does little due to everything being digested already
Ruminants - TONS

Fermentation of CHO can occur:

  • dietary fibre
  • undigested starch
  • lactose (lactose intolerant)
182
Q

What can be absorbed in the colon?

A

Not ideal

  • lack of SA
  • lack of specialized transporters

however, water, electrolyes and nutrients can be absorbed

183
Q

How is water and electrolytes absorbed in the colon?

A
  • Na+ actively absorbed (NOTE: aldosterone receptors are found in colon)
  • Cl and H2O follows
  • paracellular K+
  • absorption of SCFA can also pull water
184
Q

What nutrients are absorbed in the colon? how?

A

By-products of fermentation

  • B vitamins
  • vit K
  • SCFA (diffuse passively) although most will remain ionized and hard to absorb)

Amino acids

  • absorption has been experimentally testest but questionable
  • more transporters in horses (hindgut fermenters)
  • very specific proteins for specific animals
185
Q

What colonic transporters assist in absorption?

A

SCFA- / HCO3 exchanger
SCFA / H+ exchanger
2Na / SCFA co transport

186
Q

What is absorbed in the colon with hindgut fermenters?

A

SCFA by mucosa

major energy source (esepcially butyrate)

187
Q

what is unique about cecal fermenters?

A 
rodents/rabbits
high metabolism 
short bacterial fermentation time
eat more frequently
high quality feeds
188
Q

What happens to microbial proteins in hind gut fermentors (they are passed the SI)? why do they do this?

A

Coprophagy

“recyclying” non absorbed nutrients (Vitk, VitB, protein, Fatty acids)

189
Q

what is cecotrophy? what species practise this?

A

important in rabbits and some rodents
cecal feces has high nutrients
softer and more mucus
consume directly from anus post defecation

190
Q

How is the avian digestive system unique?

A
  • shorter and lighter
  • no teeth
  • sight for fermentation is smaller

Crop: dilation of esophagus for storage and regurgitating feed for offspring, in some pregastric fermenters

Proventriculus: glandular portion secretes mucus, pepsinogen and HCl

Ventriculus/gizzard: muscular for mechanical digestion, assisted with grit (myoglobin gives dark red appearance)

191
Q

What is unique about the SI of birds?

A

shorter but similar to mammal b/c pancreatic enzymes, bile action, absorption etc.

most have 2 ceca, some have 1 some have none.

192
Q

What is unique about colon in birds?

A

peristalsis and reverse peristalsis will move contents to ceca for last little bit of fermentation
high fibre diets utilize this for SCFA

colon terminates in cloaca
- reverse peristalsis back into colon can increase water absorption

193
Q

What something to keep in mind about birds and reptile digestive systems?

A

high amount of variability, diet dependent

194
Q

how is B12 absorbed in the ileum?

A

intrinsic factor from parietal cells in stomach binds to b12 and facilitates its absorption via specific transporters

195
Q

What 2 ways is Ca absorbed?

A

transcellular: expression of apical Ca channels, Ca enters and binds to Ca binding proteins and Ca ATPase pump pumps it out of basolateral side (Na out) all when Vit D binds to intracellular receptors

Paracellular: if Ca concentration s are high enough can flow across tight junctions (VitD independent)
occurs in duodenum after milk ingestion

196
Q

What two ways is phosphate absorbed (HPO4-)?

A

transcellular: across apical surface with co-transport of sodium (transporters are expressed by VitD)
Paracellular: across tight junctions if concentrations are high

197
Q

What electrolytes and fluids are secreted in each area of the GIT

A

Saliva: H20, HCO3,Na,Cl,K,PO3,mucus, amylase
Stomach: pepsinogen, Hcl, intrinsic factor, mucus
Pancreas: NaHCO3, amylase
Liver: Bile
SI:
Colon: mucus, water, bicarb (water and electrolytes absorbed)

198
Q

how do parietal cells, pancreatic cells and intestinal epithelium gain their ions and where are they secreted?

A

parietal cells: ions, bicarb lost in lumen, gained from blood
Pancreatic cells: bicarb from blood into lumen
epithelial cells: ions from lumen into blood

199
Q

Explain the net gain/loss of water and other substances in the GI?

A

little overall loss of water despite all the watery secretions
mucous, protein(enzymes) and bile salts are reabsorbed

200
Q

What are two common clinical problems with the GI tract?

A

Constipation and diarrhea

201
Q

What are some remedies for constipation?

A
  • lubricants (mineral)
  • motility modifying drugs that increase cholinergic affects (dont work because you have to coordinate the whole GI tract)
  • stimulant laxatives: irritate lining or alter ion channels causing electrolyte loss into lumen (Exlax - super intense)
  • hyperosmotic laxatives: draw fluid into GI lumen to stimulate motility (sodium phosphate enema, lactulose, polyethylene glycol; common in vetmed)
  • bulk laxatives: nonabsorbed callulose will draw water (metamucil, prunes, pumpkin)
202
Q

why is problematic about using sodium phosphate enemas in cats?

A

can cause hypophosphotemia

203
Q

What is diarrhea and what can it lead to?

A

inability to absorb sufficient water and electrolytes from the lumen

can cause

  • metabolic acidosis due to loss of NaHCO3 secreted by pancreatic and bile duct
  • dehydration occurs due to loss of fluid
  • severe dehydration leads to hypovolemia
  • may further lead to tachycardia
204
Q

What are 3 causes of diarrhea?

A 
#1 motility disturbances
#2 osmotic diarrhea
#3 loss of surface area
205
Q

What is motility disturbance diarrhea?

A

changes in motility that leads to transit diarrhea
from active parasites or toxins
immune stimulation can increase motility and secretion to clear parasite
more rapid and forceful contraction of smooth muscle
IgE receptors in mucosal mast cells degranulation will activate ENS to stimulate motor neurons

acute and rare, likely wont impact secerely

206
Q

What is IBS? how can we test for it?

A

thickened mucosa due to immunologic infiltration
- lymphocytes and antibodies in mucosa/submucosa
subsequent stimulation of ENS, increase motility, decreased nutrient absorption

test: endoscopy and biopsy (invasive and risky)

207
Q

Can lack of GI motility cause diarrhea?

A

yes, mixing contractions are decreased but peristaltic contractions still occur, no time for water absorption

208
Q

What is osmotic diarrhea?

A

excess or unabsorbed ingested osmotic particles
abnormal digestions of normal nutrients can lead to these particles
e.g. glycerine, sorbitol, aspartame
crystal lite slurpee example

209
Q

How can entertoxigenic e.coli cause osmotic diarrhea?

A

e.coli binds to enterocyte which leads to calcium release in the cytoplasm
Ca binds to calmodulin complex and blocks Na/Cl transporter
sodium and Cl dont get absorbed water is stuck in the lumen with them
= diarrhea

210
Q

what is secretory osmotic diarrhea?

A

hypersecretion of osmotically active particles into lumen

e.g. cholera causes choride hypersecretion from mucosal crypt cells

211
Q

Why does loss of surface area cause diarrhea?

A

villi, microvilli, plicae get destroyed and the submucosa and mucosa thickens as it gets infiltrated,

results in decreased absorption absorption of nutrients and water

212
Q

What are chronic and acute examples of damage to SA diarrhea?

A

chronic: Johne’s disease, IBS
Acute: rotavirus, coronavirus, parvovirus

strips down and sloughed off mucosa

213
Q

How can we treat diarrhea?

A

fluid therapy (IV, SubCut or intraperitoneal)

oral rehydration therapy

214
Q

What is fluid therapy?

A

injection of fluid and electrolytes (Na, Cl, K)

e.g. lactate ringers, saline, Calf-Lyte, Glycine, sodium acetate

215
Q

in what ways can the fluid and electrolytes entering the mucosal cell be maximized?

A 
Na channels
Maximized with Co transport:
Na-glucose co-transporter (SGLT11)
Na-amino acid co transport
Na/H exchanger
216
Q

What substances can be used for co-transport of electrolytes out of lumen?

A

glucose/dextrose

glycine, glutamine, alanine

217
Q

How can we treat acid/base disturbance with diarrhea?

A

bicarbonate to treat acidosis
metabolizable substrates that produce bicarb
e.g. citrate, propionate, acetate use up H+ ions to create basic products

218
Q

Ideally you give iso-osmotic (300mOsm/L) solution or mildly hyperosmotic (600mOsm/L) why is greater than 700 problematic?

A

can cause osmotic diarrhea
more sensitive if intestine is already damaged
hypertonic solutions decrease motility
- gastric/abomasal emptying rate decreases in calves = bloat

219
Q

Drug therapies with diarrhea?

A

bismuth subsalicylate, activated charcoal, loperamide (immodium, increases segmentation decreases propulsion), antimicrobials (debatable, can cause bacteria by disturbing flora)

GI Physiology (2 decks)

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