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ACVIM Reading List > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

What are the layers of the GI wall?

A
  1. Serosa
  2. Longitudinal smooth muscle layer
  3. Circular smooth muscle layer
  4. Submucosa
  5. Mucosa (bundles of smooth muscle fibers)
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2
Q

What are slow waves in the GIT?

A

Rhythmic contractions - determine by frequency of slow waves (NOT AP but slow undulating changes in resting membrane potential)
Varies along GIT

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3
Q

What cells are consider the electrical pacemakers for smooth muscle cells?

A

Interstitial cells of Cajal - Undergo cyclic change in membrane potential
Unique ion channels that periodically open = inward pacemarkers currents

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4
Q

Do the slow waves in the GIT cause muscle contraction?

A

NO! Except in stomach. Provide electrical background to allow AP when excited by intermittent spike potentials (which excites muscle contractions)

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5
Q

What are spike potentials in GIT?

A

True AP - Each time peaks of slow waves temporarily more + spike potentials = Peaks

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6
Q

In the nerve fibers how are AP generated?

A

By rapid entry of Na into nerve through Na channels

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7
Q

How are the action potentials different in the GIT?

A

Calcium-sodium channels = Much slower to open/close = Longer duration of AP

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8
Q

What are the 3 main actions that can result in depolarization of smooth muscle cells in GIT?

A
  1. Stretching of muscle
  2. Stimulation by acetylcholine release from parasympathetic nn
  3. Stimulation by several specific GI hormones
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9
Q

What are the effects of norepinephrine and epinephrine on GIT nerves (stimulation of smpathetic nn)?

A

More negative = Hyperpolarized (less excitable)

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10
Q

What causes Ca to enter the muscle fiber to result in a contraction?

A

Slow waves do NOT cause Ca to enter (ONLY Na), thus no muscle contraction alone
During a spike potential (generated by slow waves) = Large amount of Ca enters = muscle contraction

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11
Q

What are tonic contractions in the GIT?

A

Continuous (not associated with slow waves) - can last mins to hours
These are in addition or instead of rhythmical contractions

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12
Q

What is the nervous system that is within the wall of the gut?

A

Enteric Nervous System

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13
Q

What are the two major plexus and what do they control?

A
  1. Myenteric Plexus (Auerbach’s): Outer plexus twn longitudinal and circular muscle layers - mainly control GI movements
  2. Submucosal Plexus (Meissner’s): Inner plexus - controls mainly GI secretions and local blood flow
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14
Q

Which plexus in GIT controls GI movements?

A

Myenteric Plexus (Auerbach’s)

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15
Q

Which plexus in GIT controls GI secretions and local blood flow?

A

Submucosal Plexus (Meissner’s)

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16
Q

What is the main difference btwn the myenteric and submucosal plexuese?

A

Myenteric Plexus = Linear chain of interconnected neurons that run the length of GIT - Control muscle activity along length of gut
Submucosal Plexus = Functions within the inner wall of each segment of intestine, sensory signal from epithelium integrate at submucosal plexus to help control intestinal secretions, local absorption, location contraction of submucosal muscle

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17
Q

What is the neurotransmitters that results in excitation in GIT?

A

Acetylcholine

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18
Q

What is the neurotransmitters that results in inhibition in GIT?

A

Norepinephrine

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19
Q

How does parasympathetic stimulation affect the ENS?

A

Increases activity of ENS

Mainly vagus nn (some through pelvic nn)

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20
Q

How does sympathetic stimulation affect the ENS?

A

Inhibits GIT activity = From T5-L2 → sympathetic chains → celiac ganglion → mesenteric ganglia (postganglion neuron bodies) → Postganglic fibers to ENTIRE GIT → Secrete norepinephrine (small amounts of epinephrine)
Inhibits intestinal smooth muscle, blocks/inhibits neurons in ENS

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21
Q

What is the gastrocolic reflex?

A

Signals from stomach to cause evacuation of colon (reflex from gut to prevertebral sympathetic ganglia back to GIT)

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22
Q

What is the enterogastric reflex?

A

Signals from colon/small intestines to inhibit stomach motility and secretions (reflex from gut to prevertebral sympathetic ganglia back to GIT)

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23
Q

What is the colonoileal reflex?

A

Reflexes from colon to inhibit emptying of ileal contents into colon (reflex from gut to prevertebral sympathetic ganglia back to GIT)

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24
Q

What is a reflex that comes from the GIT to spinal cord/brain and then back to GIT?

A

Defecation reflexes = from colon/rectum to spinal cords and back to produce powerful colon, rectal, and abdominal contractions = Defecation

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25
Q

Where is gastrin produced?

A

G cells from antrum, duodenum, jejunum

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26
Q

What are the 2 actions of gastrin?

A

Stimulates:

  1. Gastric acid secretion
  2. Growth of gastric mucosa
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27
Q

Name 3 stimuli that result in secretion of gastrin?

A
  1. Protein
  2. Distension
  3. Nerve (gastrin releasing peptide from vagal stimulation)
    Acid = Inhibits release
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28
Q

Where is cholecystokinin secreted?

A

I cells of duodenum, jejunum, and ileum

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29
Q

Name 3 stimuli that result in secretion of cholecystokinin?

A
  1. Protein
  2. Fat
  3. Acid
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30
Q

Name 6 roles of cholecytsokinin.

A 
Stimulates:
1.  Pancreatic enzyme secretion
2.  Pancreatic bicarbonate secretion
3.  BG contraction
4.  Growth of exocrine pancreas
Inhibits:
5.  Gastric emptying (moderate - time for digestion)
6.  Appetite (sensory afferent in duodenum via vagus to appetite centers)
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31
Q

Where is secretin secreted from?

A

S cells from duodenum, jejunum, ileum

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32
Q

What are 2 stimuli for secretion of secretin?

A
  1. Acid

2. Fat

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33
Q

Name 4 things that are stimulated and 1 thing that is inhibited by secretin.

A 
Stimulates:
1.  Pepsin secretion
2.  Pancreatic bicarbonate secretion!!! (neutralizes acidic contents)
3.  Biliary bicarbonate secretion
4.  Growth of exocrine pancrease
Inhibits:
1.  Gastric Acid secretion
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34
Q

What cells secrete gastric inhibitory peptide (GIP)?

A

K cells of duodenum and jejunum

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35
Q

What are 3 stimuli for gastric inhibitory peptide (GIP) secretion?

A
  1. Protein
  2. Fat
  3. Carbohydrates (less)
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36
Q

Name 1 thing that is stimulated and 2 things that are inhibited by gastric inhibitory peptide (GIP)?

A 
Stimulates:
1.  Insulin release
Inhibits:
1.  Gastric motility (mild)
2.  Gastric Acid Secretion
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37
Q

What is another name for gastric inhibitory peptide (GIP)?

A

Glucose-dependent insulinotrophic peptide

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38
Q

Which cells secrete motilin?

A

M cells of stomach, duodenum, jejunum

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39
Q

Name 3 things that stimulate the secretion of motilin.

A
  1. Fat
  2. Acid
  3. Nerve
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40
Q

What does motilin do in GIT?

A

Stimulates gastric and intestinal motility (cyclic release = waves → interdigestive myoelectrical complexes

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41
Q

What are the 2 types of movement in the GIT?

A 
Propulsive movements (food to move to accommodate digestion/absorptive)
2.  Mixing movements (of contents)
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42
Q

What are the stimuli for propulsive movements = peristalsis in GIT?

A

Stimulus = Distenstion (stretching) caused by material

Some chemical and physical irritation, strong parasympathetic nervous signals

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43
Q

What is the function of the myenteric plexus in peristalsis?

A

If no myenterix plexus (congenital) peristalsis will NOT occur
Block it with atropine (affecting cholinergic nn in myenteric plexus)

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44
Q

Why are the directional movements of peristalic waves to the anus?

A

Can occur in either direction, but orad dies out = likely related to polarization of myenteric plexus

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45
Q

What is the “law” of the gut?

A

Peristaltic reflex = gut reflexes to result in receptive relaxation (easier propulsion) - Perstaltic waves to the anus

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46
Q

Name 2 mixing movements in the GIT?

A
  1. Peristalsis again sphincter = churning of content

2. Local intermittent constrictive contractions within gut wall (chopping and shearing contents)

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47
Q

What is splanchnic circulation?

A

• Blood flow in gut, spleen, pancreas → liver (via portal vein) → hepatic sinusoids (reticuloendothelial cells to remove bacteria, carbs and proteins absorbed) → hepatic veins → vena cava

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48
Q

Which nutrient is NOT carried in portal blood and why?

A

o Fats absorbed from GIT (not carried in portal blood) into intestinal lymphatics to thoracic duct to systemic circulation

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49
Q

What are the 3 phases of swallowing?

A
  1. Voluntary Stage (bolus into pharynx)
  2. Pharyngeal Stage (involuntary)
  3. Esophageal Stage (involuntary)
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50
Q

What are the 2 types of peristalsis during the esophageal phase?

A
  1. Primary peristalsis - continuous wave from pharynx

2. Secondary Peristalsis = from distension of esophagus (controlled by myenteric NS)

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51
Q

What are the 3 main motor functions of the stomach?

A
  1. Storage of food until into SI
  2. Mixing of food with gastroc secretions into chyme
  3. Slow empyting of chyme from sotmach into SI
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52
Q

What results in relaxation of stomach during the storage function of the stomach?

A

Distension with food → “vasovagal reflex” to brain stem → relaxes stomach wall (to accommodate more food)

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53
Q

Describe the basic electrical rhythm of the stomach.

A

Mixing waves = Slow waves (spontaneous) that result in mixing of the food (chyme), more intense at antrum

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54
Q

What are hunger contractions?

A

When the stomach as been empty for hours - Rhythmic powerful contractions

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55
Q

What controls stomach emptying?

A

“Pyloric pump” - intense peristaltic wave in the antrum, pyloric sphincter also controls this

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56
Q

In general what regulates stomach emptying?

A

Signals from stomach and duodenum (potent)

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57
Q

What are the 2 gastric factors that control stomach emptying?

A

Promote emptying = increased pyloric pump

  1. Gastric food volume (stretch)
  2. Gastrin release
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58
Q

What are the 2 duodenal factor that control stomach emptying?

A

Inhibit Emptying

  1. Enterogastric Relfex (food in duodenum inhibit pyloric pump)
  2. Hormones = CCK (from jejunal cells that sense fat) = Blocks stomach motility (caused by gastrin)
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59
Q

What are the 2 major movements in the SI?

A
  1. Mixing contractions = segmentation contractions (from SI distension with chyme)
  2. Propulsive Movements = Perstaltic waves
    Stretch (chyme in duodenum), gastroenteric reflex, hormones (gastrin, CCK, insulin, motilin, serotonin)
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60
Q

Which hormones increased motility in SI?

A

gastrin, CCK, insulin, motilin, serotonin

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61
Q

Which hormones decreased motility in SI?

A

Secretin and glucagon

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62
Q

What is the gastroielal reflex?

A

After a meal = increased peristalsis in ileum = emptying

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63
Q

What are the 2 major movements of the colon?

A
  1. Mixing movements - large circular contractions

2. Propulsion movements = MASS MOVEMENTS (dt gastrocolic and duodenocolic reflexes = distension)

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64
Q

What are the 2 reflexes that control defecation and which one is “stronger”?

A
  1. Intrinsic Reflex (local ENS - myenteric plexus)

2. Parasympathetic Defecation Relfex (via pelvic nn) = VERY POWERFUL peristalsis and inhibits internal anal sphincter?

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65
Q

Which anal sphincter is under voluntary control?

A

External anal sphincter

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66
Q

Which nerves control the parasympathetic defecation reflex?

A

Pelvic nn

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67
Q

What is the peritoneointstinal reflex?

A

irritation of peritonenum = intestinal paralysis

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68
Q

What is renointestinal reflex and vesicointestinal reflex?

A

Inhibits intestinal activity due to kidney or bladder irritation

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69
Q

What are the two layers of muscles in the GIT?

A
  1. Circular muscles

2. Longitudinal muscles

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70
Q

What is the name of gastrin secreting tumors?

A

Zollinger-Ellison Syndrome within the pancreas

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71
Q

What is a unique feature of the electrical activity of GIT smooth muscle?

A

Slow waves = Not AP but oscillating depolarization and repolarization

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72
Q

What is the action potential in GIT dependent on?

A

Action potentials in GIT cannot occur unless the slow wave brings the membrane potential to threshold

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73
Q

What determines the rate and action potentials and contractions in various segments of GIT?

A

The frequency of slow waves which is controlled by pacemaker = Interstital cells of Cajal

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74
Q

What type of channels control the depolarization and repolarization of the slow waves in GIT?

A

Ca 2+ open resulting in Ca2+ entering cell = Depolarization

K+ open resulting in K+ OUT of cell = Repolarization

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75
Q

What do neural and hormonal input influence in GIT?

A

Neural input and hormonal input DO NOT influence the frequency of slow waves, they do influence the frequency of action potentials

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76
Q

During fasting what type of gastric contraction periodically occurs?

A

Migrating myoelectric complexes = mediated by motiliin

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77
Q

What is another name for pits?

A

Crypts of Lieberkuhn = Secretory cells in GIT

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78
Q

What are the basic steps in secretion from a glandular cell in the GIT?

A
  1. Diffusion of substance from capillaries into glandular cell
  2. Secretory substance made in ER
  3. Formed by ribosomes and Golgi
  4. Stored Glogi vesicles
  5. Increased permeability = Increased intracellular Ca2+ = Vesicles fuse to apical membrane = Exocytosis
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79
Q

What is mucus made of?

A

Water, electrolytes, glycoproteins

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80
Q

What are the 6 magic properties of mucus?

A
  1. Adheres tightly to food and spreads thin
  2. Sufficient body to coat GIT so that food rarely touches mucosa
  3. Causes formation of fecal balls
  4. Resistant to digestion by digestive enzymes
  5. Particles slide along it easily
  6. Amphoteric properties (can buffer acid or alkali)
81
Q

What are the 2 types of secretions from salivary glands?

A
  1. Serous = Ptyalin (a-amylase) = Digest starch

2. Mucus = Mucin = Lubrication

82
Q

What is ptyalin?

A

a-Amylase to digest starches, found in salivary secretions are part of serous secretion

83
Q

What is the primary secretion from salivary glands?

A

Either ptyalin or muscus with same electrolyte composition as ECF

84
Q

What is the final composition of saliva and where do these changes take place?

A

Within the salivary ducts = HIGH K+ and HCO3- (little Na and Cl)

  1. K+ active secretion
  2. HCO3- secretion
  3. Na active absorption
  4. Cl- passive absorption (follows Na)
85
Q

What components are in salivary to attack bacteria?

A
  1. Thiocyanate ions
  2. Lysozyme
  3. Ig
86
Q

What is the primary nerous control of saliva?

A

Parasympathetic = 2 salivary nuclei in brainstem

Stimulated by high centers (appetite) or something on tongue

87
Q

Discuss the blood flow in the salivary glands.

A

The salivary glands make kalikrein - which when secreted splits a-2 globulin into bradykinin = VASODILATION

88
Q

What is the primary secretion in the esophagus?

A

MUCUS for Lubrication (simple and compound mucous glands)

89
Q

What are the two major glands in the stomach and what do each of them secrete?

A
  1. Oxyntic Gland (Gastric Gland) = HCl, Pepsinogen, intrinsic factor, mucus
  2. Pyloric Gland = Mucus, Gastrin
90
Q

What are the 3 main cell types that make of the gastric/oxyntic gland and what do they secrete?

A
  1. Mucous Neck Cell = Mucus
  2. Oxyntic/Partiel Cells = HCl, intrinsic factor
  3. Peptic/Chief Cells = Pepsinogen
91
Q

What is the driving force behind secretion of HCl from the oxyntic/parietal cells?

A

H+/K+ ATPase pump on the apical membrane that results in secretion of H+ intot he canaliculus

92
Q

What are the steps in HCl secretion in a oxyntic/parietal cells?

A
  1. Water dissociates into H+ and OH- in the cytoplasm
  2. H+/K+ ATPase allows H+ to be secreted into the canaliculi
  3. Potassium in brought into the cell on the basolateral membrane by a Na+/K+ ATPase pump, this makes low intracellular Na+, which brings Na+ into the cell from the canaliculus
  4. Pumping out of H+ allows formation of HCO3- since OH- is accumulating in the cell cytoplasm, this is mediated by carbonic anhydrase, this is then secreted in exchange for Cl-, which is sent out into the canaliculus to meet with H+ and make HCl
  5. Water passes into the canaliculus by osmosis
93
Q

What are the 3 main stimuli for HCl secretion and which cells do these substances stimulate?

A
  1. Acetylcholine = All cells are stimulated
  2. Gastrin = Only parietal cells are stimulated
  3. Histamine = Only parietal cells are stimulated
94
Q

Which cell type secretes HCl?

A

Oxyntic/parietal cells (part of gastric/oxyntic gland)

95
Q

Which cell type secretes intrinsic factor (dog)?

A

Oxyntic/parietal cells (part of gastric/oxyntic gland)

96
Q

Which cell type secretes pepsinogen?

A

Peptic/Chief cells (part of gastric/oxyntic gland)

97
Q

How is pepsinogen activated?

A

Pepsinogen (inactive) is secreted by the peptic/chief cells in the gastric/oxyntic gland. This is converted to pepsin (ACTIVE = highly proteolytic at low pH) when HCl is present

98
Q

What stimulates the conversion of pepsinogen into pepsin?

A

HCl

99
Q

What are the 2 main stimuli for secretion of pepsinogen from peptic/chief cells?

A
  1. Acetylcholine (vagus n. and gastric enetric plexus)

2. Acid in the stomach

100
Q

What does ECL cells stand for?

A

Enterochromaffin-Like cell (ECL cell)

101
Q

Which cell type does the parietal cells in the gastric glands work closely with?

A

ECL cells

102
Q

What do the ECL cells secrete that results in the parietal cells secreting HCl and what controls this process?

A

Rate and amount of HCL produced is directly related to histamine from ECL cells, which is controlled by GASTRIN

103
Q

Which cells make gastrin?

A

G cells in the pyloric glands in the distal end of the stomach

104
Q

When the G cells in the pyloric glands sense that there is a protein rich meal what occurs?

A

G cells are stimulated by protein to release GASTRIN into the blood to reach the ECL cells, which when stimulated by gastrin will release HISTAMINE which results in HCL release from the parietal cells

105
Q

Which secretagogue is the most important in gastric acid secretion?

A

Histamine!

106
Q

What are the 3 phases of gastric secretion and how much do they account for acid secretion?

A
  1. Cephalic Phase = 30% acid production
  2. Gastric Phase = 60% acid production
  3. Intestinal Phase = 10% acid production
107
Q

What controls the cephalic phase of gastric secretion?

A

Sight, smell, taste of food → HCl + pepsin release
Controlled by:
Cerebral cortex (appetite center amygdala and hypothalamus) → Vagus n. → Stomach via Acetylchoine
G cells →Gastrin Releasing peptide = GASTRIN release

108
Q

What controls the gastric phase of gastric secretion?

A 
Food in stomach (stretch) = HCl release
Controlled by:
Long vagovagal reflex = acetylcholine
Local enteric reflex 
Peptides and AA → G cells → GASTRIN
109
Q

What controls the intestinal phase of gastric secretion?

A

Food in duodenum
Controlled by:
Enterooxyntic (not gastrin per CVT??)

110
Q

How is gastric secretion inhibited?

A

Food in SI

  1. Reverse enterogastric reflex (myeneteric NS, sympathetic NS, vagus n)
  2. Food in SI stimulates secretion of SECRETIN and 3 other inhibitors (gastric inhibitory peptide, somatostatin, vasoactive intestinal peptide)
111
Q

What happens in the stomach glands between meals?

A

They make mucus, almost NO acid!

112
Q

What is the pancreatic duct and which species have it?

A

Opens within bile duct at major duodenal papilla
Dogs = Usually (smaller, but can be absent)
Cats = ALWAYS!

113
Q

What is the accessory pancreatic duct and which species have it?

A

Opens into duodenum at minor duodenal papilla
Dogs = ALWAYS!
Cats = Occasionally

114
Q

What are the two main functions of pancreatic secretions?

A
  1. Digestive enzymes

2. Na bicarbonate

115
Q

How are pancreatic enzymes secreted?

A

Pancreatic enzymes are secreted as zymogens (INACTIVE form) - Such as trypsinogen
Once into the small intestine they are activated = Trypsin

116
Q

Which pancreatic enzyme can activate all the other pancreatic enzymes?

A

Trypsin

117
Q

What 3 pancreatic enzymes are responsible for protein digestion?

A
  1. Trypsin!!!!
  2. Chymotrypsin
  3. Carboxypolypeptide (can release AA)
118
Q

What pancreatic enzyme is responsible for carbohydrate digestion?

A

Pancreatic amylase (starch into disaccharides and trisaccharides)

119
Q

What 3 pancreatic enzymes are responsible for fat digestion?

A 
Pancreatic lipase (fat into FA and monglycerides)
Cholesterol esterase (hydrolysis of cholesterol)
Phospholipase (FA splits from phospholipids)
120
Q

What enzyme is made in pancreatic acini that helps to prevent autodigestions and were is it present?

A

Trypsin Inhibitor

Prevents activation of zymogens in pancreas or ducts or intracellular

121
Q

Which cells in the pancreas make bicarbonate?

A

Epithelial cells that line the ductules and ducts

Role of bicarbonate is to neutralize acid from stomach chyme

122
Q

What are the steps in making bicarbonate in the pancreas?

A
  1. CO2 diffuses into the cell from the blood, combines with water to form carbonic acid (H2CO3), dissociates into H+ and HCO3-
  2. H+ is traded in the blood for Na+, which is transported out of the cell with HCO3-
  3. This also pulls water by osmosis
123
Q

What are the 3 main stimuli for pancreatic secretion?

A
  1. Acetylcholine
  2. Cholecystokinin (CCK)
  3. Secretin
124
Q

Which hormones control release of pancreatic fluid and bicarbonate?

A

Secretin

125
Q

Which hormones control release of pancreatic digestive enzymes?

A 
Vagal stimulation (acetylcholine)
Cholecystokinin (CCK)
126
Q

What stimulates the release of acetylcholine that results in pancreatic secretions?

A

Vagus n. and ENS stimulation

127
Q

What stimulates the release of cholecytskinin (CCK) that results in pancreatic secretions?

A

Released from duodenum and upper jejunum from I cells in response to protein or AA in the lumen

128
Q

What stimulates the release of secretin that results in pancreatic secretions?

A

Released from duodenum and jejunum in response to acidic content of chyme in the lumen

129
Q

What is important about the 3 stimuli that result in pancreatic secretions?

A

The stimuli potentate each other, meaning that pancreatic secretion is greatest with the combined stimuli as compared to single stimuli

130
Q

What are the 3 phases of pancreatic secretion?

A

Same as gastric secretion

  1. Cephalic = 20% pancreatic enzymes
  2. Gastric = 5-10% pancreatic enzymes
  3. Intestinal: LOTS of pancreatic fluid and bicarbonate (secretin); 70-80% pancreatic enzymes (CCK)
131
Q

What controls the cephalic phase of pancreatic secretion?

A

Acetylcholine (vagal n.) = 20% pancreatic enzymes (BUT NO fluid)

132
Q

What controls the gastric phase of pancreatic secretion?

A

Acetylcholine (vagal n.) = 5-10% pancreatic enzymes (BUT NO fluid)

133
Q

What controls the intestinal phase of pancreatic secretion?

A
  1. Chyme in SI (acid) → Secretin (from S cells in duodenum) → Lots of pancreatic fluid and bicarbonate
  2. Food in SI (peptides/fat) → CCK (from I cells in duodenum and upper jejunum) → 70-80% pancreatic enzymes
134
Q

What are the two main roles of bile?

A
  1. Fat digestion and absorption (based on bile acids/salts that aid in emulsifying and absorbing fats)
  2. Excretion of waste (including bilirubin and cholesterol)
135
Q

What are the two stages of bile secretion?

A
  1. Bile is secreted by hepatocytes into bile canaliculi
  2. Bile flows through ducts to the hepatic duct → common bile duct → duodenum OR cystic duct to Gallbladder
    Along the way in the ductules/ducts watery Na+ and HCO3- solution secreted by secretory epithelial cells (stimulated by secretin)
136
Q

Which hormones results in secretion of watery Na+ and HCO3- solution from secretory epithelial cells during the second stage of bile secretion?

A

Secretin!! Which is stimulated by presence of acid within the duodenum

137
Q

What happens to bile when it is stored in the GB?

A

The bile is concentrated (Water, Na+, Cl- are absorbed through the wall of the GB) - via active transport of Na+ and passive movement of others = Concentration of bile salts, cholesterol. Lecithin, bilirubin

138
Q

What are the two imperative steps in emptying the GB and what controls this?

A

Need contraction of GB and relaxation of Sphincter of Oddi (at exit of common bile duct into duodenum)
This is stimulated by CCK that is released in response to a fatty meal in the duodenum

139
Q

How are bile salts made?

A

From cholesterol (diet or made in liver) → 1. cholic acid OR 2. Chenodeoxycholic acid → These combine with either 1. Glycine or 2. Taurine → Conjugated bile salts

140
Q

What are the two main roles of bile salts?

A
  1. Emulsifying or detergent function (decrease surface tension, allows GIT to break down fats)
  2. Absorption of micelles into blood (MAJOR effect! = fatty acids, monoglycerides, cholesterol, other lipids)
141
Q

What 4 components are absorbed via micelles with bile salts?

A
  1. Fatty Acids
  2. Monglycerides
  3. Cholesterol
  4. Other Lipids
142
Q

Explain enterohepatic circulation of bile salts?

A

Bile salts are reabsorbed in SI (diffusion and active transport) → Portal blood → Liver venous sinusoids → Hepatocytes → Bile
About 94% of bile salts are recirculated (up to 17x)

143
Q

What are the 2 main glands in the SI that result in secretions?

A
  1. Brunner’s glands = Mucus and bicarbonate

2. Crypts of Lieberkuhn = Digestive Juices (mucus and watery vehicle)

144
Q

What are the Brunner’s gland stimulated by in the SI?

A

Result in mucus and bicarbonate secretion
Stimulated by: food, vagal stimulation, secretin
Result in protection of mucosa in duodenum

145
Q

What are the two main cells types of the Crypts of Lieberkuhn?

A
  1. Goblet Cells = Mucus

2. Enterocytes = Absorb and secrete water and electrolytes (PURE ECF, alkaline fluid)

146
Q

How dot he enterocytes of the Crypts of Lieberkuhn result in formation of a watery vehicle?

A
  1. Active secretion of Cl-
  2. Active secretion of HCO3-
    Drags along Na+ and water
147
Q

What are the main villus enzymes?

A
  1. Peptidase (peptides → AA)
  2. Sucrase, maltase, isomaltase, lactase (dissaccharides → monosaccharides)
  3. Intestinal lipase (fats → glycerol and FA)
148
Q

Does the large intestinal have villi and Crypts of Lieberkuhn?

A

No villi

Yes - Crypts of Lieberkuhn

149
Q

What is the major component of the Crypts of Lieberkuhn in the large intestine?

A

MUCUS (some bicarbonate) - Lubrication and hold feces together

150
Q

Why is saliva hypotonic?

A

Active net solute absorption and salivary ducts are impermeable to water

151
Q

Why is neural stimulation of the salivary glands unique?

A

They are controlled by both parasympathetic and sympathetic NS

152
Q

What are the net results of gastric parietal cells?

A

Net secretion of HCl and net absorption of HCO3- (alkalaine tide that is seen after meals)

153
Q

What are the 3 main stimulators of H+ secretion on parietal cells and what are their receptors?

A
  1. ACh (From Vagus n, M3 receptor)
  2. Gastrin (From G cells in antrum, CCKb receptor)
  3. Histamine (From ECL cells, H2 receptor)
154
Q

What is the MOA of PPI, omeprazole?

A

Inhibit the H+/K+ ATPase on the apical membrane of the gastric parietal cell

155
Q

Name the 2 primary bile acids.

A

Cholic acid and chenodeoxycholic acid

156
Q

Name 2 enzymes that aid in starch digestion that are not found in intestinal epithelium.

A
  1. Salivary alpha amylase (Ptyalin)

2. Pancreatic amylase

157
Q

What enzymes and where are disacchardies hydrolyzed into monosaccharides?

A

Intestinal Epithelial Enzymes - Within villi in the brush border

  1. Maltase
  2. Alpha-Dextrinase
  3. Lactase
  4. Sucrase
158
Q

What does lactase do?

A

Splits Lactose into galactose and glucose

159
Q

What does sucrose do?

A

Splits sucrose into fructose and glucose

160
Q

What does maltose and other 3-9 glucose polymers split into?

A

Glucose by maltase and alpha-dextinase

161
Q

What are the final products of carbodyhrate digestion?

A

Monosaccarides that are absorbed immediately into portal blood

162
Q

What 3 locations do carbohydrate digestion occur?

A
  1. Mouth
  2. Small intestine (pancreatic secretions)
  3. Villi (Brush border)
163
Q

What is the most important function of pepsin?

A

Digestion of collagen (to allow digestion of other cellular proteins)

164
Q

Name 3 places that protein digestion occurs?

A
  1. Stomach
  2. Duodenum/Upper jejunum (pancreatic secretions)
  3. Enterocytes (duodenum and jejunum)
165
Q

What is the final product of protein digestion?

A

Amino Acids

166
Q

What is the enzyme in the stomach that aid in protein digestion?

A

Pepsin

167
Q

What are the enzymes in the duodenum/upper jejenum that aid in protein digestion?

A

Pancreatic enzymes: Trypsin. Chymotrypsin, carboxypolypeptidase, proelastase

168
Q

What is the enzyme in the enterocytes that aids in final polypeptide and amino acid digestion?

A

Peptidases (aminopolypeptidase, dipeptidase)

169
Q

What is the most important enzyme of fat digestion?

A

Pancreatic lipase (little by enteric lipase)

170
Q

What is the final product of fat digestion?

A

Fatty acids and 2-monoglycerides

171
Q

What are essential for emulsification of tryglycerides?

A

Bile salts and lecithin

172
Q

By what process is water absorbed in the small intestine?

A

Entirely by diffusion

173
Q

What is the main mechanism of ion absorption in SI?

A

Active transport of Na+
Na+ is actively transported from basolateral membrane into interstitial space Low intracellular conc of Na → electrochemical gradient → therefore more Na moves from chyme into enterocyte

174
Q

What are the 3 final monosaccharides?

A
  1. Glucose
  2. Galatose
  3. Fructose
175
Q

What is another name for the Na+/glucose cotransporter in the SI?

A

SGLT 1

176
Q

Which transporter is located on the basolateral surface to transport glucose, galactose, and fructose into the blood?

A

GLUT 2

177
Q

Which transporter on the apical surface allows for facilitated diffusion of fructose?

A

GLUT 5

178
Q

Which enzyme in the brush border in the SI converts trypsinogen into trypsin?

A

Enterokinase

179
Q

What are the 2 main ways that proteins are absorbed in the SI?

A

Via Na+ co-transporter or less by facilitated diffusion

180
Q

Name the 4 fat soluble vitamins.

A

Vitamins A, D, E, K

181
Q

What are the 4 steps of Vitamin B12 absorption?

A
  1. Dietary B12 released from pepsin (stomach)
  2. Free B12 binds to R protein (from saliva)
  3. Duodenum: Pancreatic proteases degrade R protein and Vit B12 transferred to intrinsic factor (prevented from degrading)
  4. Vit B12-Intrinsic Factor Complex - Ileum it is transported
182
Q

What is the major site of Na+ absorption in the SI?

A

Jejunum

183
Q

What occurs in the colonocytes for Na and K?

A

Na+ absorption (+++aldosterone)

K+ secretion

184
Q

What are 2 main things that are lost in diarrhea?

A

HCO3- and K+ = Hypercholermic metabolic acidosis

185
Q

What is the main electrolyte that is secreted by enterocytes?

A

Cl- (based on increased cAMP). Na+ and water follow = secretion

186
Q

What are the 2 main blood supplies for the liver?

A

Portal vein and hepatic artery

187
Q

What accounts for the huge regenerative capacity of the liver?

A

HGF (Heptocyte growth factor) produced by mesenchymal cells

188
Q

What is the name of the reticuloendothelial cells in the liver?

A

Kupffer cells

189
Q

What are the 3 things in the portal triad?

A
  1. Portal Vein
  2. Bile Duct
  3. Hepatic Artery
190
Q

What are the areas that lymph is created/filtrated in the liver lobules?

A

Within the Space of Disse

191
Q

What are the 4 main functions of the liver in carbohydrate metabolism?

A
  1. Store glycogen (glucose buffer)
  2. Convert galactose/fructose into glucose
  3. Gluconeogenesis
192
Q

What are the 3 main functions of the liver in fat metabolism.

A
  1. High rate of oxidation of fatty acids (fats → glycerol + FFA → Beta oxidation →Acetyl CoA→TCA Cycle or acretoacetic acid
  2. Synthesis cholesterol (for bile salts), phospholipids (cell membranes), lipoproteins
  3. Convert carbs and proteins into fat
193
Q

What are the 4 main functions of the liver in protein metabolism?

A
  1. Deamination of AA
  2. Formation of urea
  3. Formation of plasma proteins (except Ig)
  4. Interconversion of AA
194
Q

Name 4 other functions of the liver in metabolism.

A
  1. Stores Vitamins - A, D, B12
  2. Blood coagulation - makes factors (needs Vit K)
  3. Storage of iron == Ferritin
  4. Metabolizes drugs, hormones, Ca2+, others
195
Q

Discuss the excretion of bilirubin.

A
  1. RBCs are degraded by reticuloendothelial system (heme + globin)
  2. Via heme oxygenase = Biliverdin
  3. Unconjugated bilirbin (bound to albumin)
  4. In liver conguates with glucuronic acid = Bilirubin glucuronide (80%) and bilirbuin sulfate (10%) = Conjugated bilirubin
  5. Conjugated bilirubin is excreted in bile into intestesines
  6. In intestines - intestinal bacteria convert it into urobilinogen
  7. About 90% of urobilinogen is converted to stercobilinogen then converted to stercobilin and is excreted in feces
  8. About 10% of urobilinogen is absorbed into blood and is either recycled to bile (about 95%) or excreted by kidney (about 5%). When urobilinogen is exposure to air in the urine it is converted to urobilin
196
Q

What would you expect with bilirubin in hemolysis?

A

Unconjugated bilirubin high

197
Q

What would you expect with bilirubin in Cholestasis?

A

Conjugated bilirubin high

198
Q

What would you expect with bilirubin in total EHBDO?

A

NO bilirbin in feces (since no stercobilin stool is light), no urobilin in urine

199
Q

How is urea formed in the urine?

A

Amino Acid + Keto acid (alpha keto-glutoric acid) gets transminated into keto acid + amino acid (glutamic acid)
Via oxiative deamination glutamic acid is converted to keto acid + NH3 (ammonia)
The ammonia combined with CO2 and creates urea!

ACVIM Reading List (27 decks)

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