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IMS: Physiology > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

GI System

Structures

A
  • Gastrointestinal Tract
    • Mouth
    • Pharynx
    • Esophagus
    • Stomach
    • Small intestine
      • Duodenum
      • Jejunum
      • Ileum
    • Large intestine
      • Colon
        • Ascending
        • Transverse
        • Descending
    • Rectum
    • Anus
  • Associated Glandular Organs
    • Salivary glands
    • Liver
    • Pancreas
    • Gallbladder
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2
Q

Splanchnic Circulation

A
  • Large blood flow
  • Serve reservoir function
    • 70% of mobilized blood during exercise
  • Gets 20-25% cardiac output at rest
    • Can increase 8x following a meal ⇒ postprandial hyperemia
  • Control of flow via both local and nervous system control
    • SNS ⇒ Norepi ⇒ α-adreneric receptors ⇒ vasoconstriction ⇒ decrease blood flow
    • Enteric NS ⇒ Ach & vasoactive intestinal peptide (VIP) ⇒ increase blood flow
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3
Q

Motility

A

The movement and mixing of GI contents.

Regulated process.

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4
Q

Secretion

A

The release of water, electrolytes, enzymes, and mucous from glands in the GI tract.

Regulated process.

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5
Q

Digestion

A

The chemical breakdown of ingested material into molecules that can be absorbed in the blood.

Mainly through enzymes and gastric acid.

Not directly regulated but enzymatic secretions are.

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6
Q

Absorption

A

The process by which nutrients are take up by mucosal cells and enter the blood stream.

Absorption not directly regulated.

Motility and secretion are which influence absorption.

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7
Q

Regulation of GI Function

A

Function regulated by three different systems:

  1. ANS
    • Sympathetic
    • Parasympathetic
    • Enteric
  2. GI hormones
  3. Paracrines
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8
Q

Vagovagal Reflexes

A

Occurs when the vagus nerve (CN-X) participiates in both afferent sensation and efferent responses without CNS involvement.

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9
Q

SNS Control

A

Sympathetic NS

  • Most fibers terminate on plexuses of enteric NS
  • Few directly innervate blood vessels (vasoconstriction) and glands
  • Norepi and Neuropeptide Y (NPY) main transmitters
  • Functions to:
    • relax wall muscle
    • constrict sphincters
    • inhibit salivary secretions (norepi)
    • inhibit intestinal secretions (NPY)
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10
Q

PNS Control

A

Parasympathetic NS

  • Most fibers terminate on enteric NS neurons
  • Stimulation of GI motility and secretion
  • Primary neurotransmitters:
    • Ach
    • Gastrin-releasing hormone
    • Substance P
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11
Q

Enteric NS Control

A

Main neural control of GI system.

  • Myenteric plexus (Auerbach’s)
    • Located between circular and longitudinal smooth muscle layers through entire GI system
    • Primarily regulates:
      • intestinal smooth muscle
      • participates in tonic and rhythmic contractions
    • Excitatory motor neurons
      • Release Ach and Substance P
      • Induce contraction
    • Inhibitory motor neurons
      • Release VIP and NO
      • Induce relaxation
  • Submucosal plexus (Meissner’s)
    • In submucosa of small and large intestine
    • Primarily regulates:
      • intestinal secretions
      • local absorptive environment
    • Release VIP and Ach
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12
Q

Acetylcholine

A
  1. Releasing Nerves
    • Parasympathetic
    • Cholinergic
  2. Innervate
    • Smooth muscle
    • Glands
  3. Functions:
    • Contracts wall muscle
    • Relaxes sphincters
    • Increases salivary, gastric, and pancreatic secretions
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13
Q

Vasoactive Intestinal Peptide

(VIP)

A
  1. Releasing Nerves
    • Parasympathetic
    • Cholinergic
    • Enteric
  2. Innervate
    • Smooth muscle
    • Glands
  3. Functions:
    • Relaxes sphincters
    • Increases pancreatic and intestinal secretions
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14
Q

Norepinephrine

A
  1. Releasing Nerves
    • Sympathetic
    • Adrenergic
  2. Innervate
    • Smooth muscle
    • Glands
  3. Functions:
    • Relaxes wall muscle
    • Contracts sphincters
    • Decreases salivary secretions
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15
Q

Neuropeptide Y

(NPY)

A
  1. Releasing Nerves
    • Sympathetic
    • Adrenergic
    • Enteric
  2. Innervate
    • Smooth muscle
    • Glands
  3. Functions:
    • Relaxes wall muscle
    • Decreases intestinal secretions
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16
Q

Gastric-releasing Peptide

A
  1. Releasing Nerves:
    • Parasympathetic
    • Cholinergic
    • Enteric
  2. Innervate:
    • Glands
  3. Functions:
    • Increases gastrin secretion
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17
Q

Substance P

A
  1. Releasing Nerves:
    • Parasympathetic
    • Cholinergic
    • Enteric
  2. Innervate:
    • Smooth muscle
    • Glands
  3. Functions:
    • Contracts wall muscle
    • Increases salivary secretions
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18
Q

Enkephalins

A
  1. Releasing Nerves
    • Enteric
  2. Innervate
    • Smooth muscle
    • Glands
  3. Functions:
    • Constrict sphincters
    • Decrease intestinal secretions
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19
Q

Cholecystokinin

(CCK)

A
  1. Releasing Cells:
    • I cells
  2. Releasing structures:
    • Pancreas
    • Gallbladder
    • Stomach
  3. Functions:
    • Increases enzyme secretion
    • Contracts gallbladder
    • Decreases gastric emptying
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20
Q

Glucose-dependent Insulinotropic Peptide

(GIP)

A
  1. Releasing Cells:
    • K cells
  2. Releasing structures:
    • Pancreas
    • Stomach
  3. Functions:
    • Releases insulin
    • Inhibits acid secretion
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21
Q

Gastrin

A
  1. Releasing Cells:
    • G cells
  2. Releasing structures:
    • Stomach
  3. Functions:
    • Increases gastric acid secretion
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22
Q

Motilin

A
  1. Releasing Cells:
    • M cells
  2. Releasing structures:
    • GI smooth muscle
  3. Functions:
    • Increases contractions
    • Increases migrating motor complexes
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23
Q

Secretin

A
  1. Releasing Cells:
    • S cells
  2. Releasing structures:
    • Pancreas
    • Stomach
  3. Functions:
    • Releases HCO3-
    • Releases pepsin
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24
Q

Hormone Distribution

A
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25
Q

Histamine

A
  1. Releasing Cells:
    • Enterochromaffin-like cells
    • Mast cells
  2. Releasing structures:
    • Stomach
  3. Functions:
    • Increases gastric acid secretion
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26
Q

Prostaglandins

A
  1. Releasing Cells:
    • Cells lining GI tract
  2. Releasing structures:
    • Mucosa
  3. Functions:
    • Increase blood flow
    • Increase mucus secretion
    • Increase HCO3- secretion
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27
Q

Somatostatin

A
  1. Releasing Cells:
    • D cells
  2. Releasing structures:
    • Stomach
    • Pancreas
  3. Functions:
    • Inhibits peptide hormones
    • Inhibits gastric acid secretion
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28
Q

GI Smooth Muscle

A
  • Smooth muscle cells electrically coupled
  • Resting membrane potential oscillates ⇒ slow waves or basic electric rhythm
  • Slow waves generated by Interstitial Cells of Cajal (ICC)
    • Located in muscularis externa
    • Connected by gap junctions to smooth muscle cells
    • Drives AP of the entire muscle
  • Amplitude & frequency of slow waves altered by:
    • ANS
      • SNS input decreases or abolishes slow waves
      • PNS input increases amplitude
    • Hormones
    • Paracrines
  • Weak contractions can occur without AP if slow wave amplitude reaches contraction threshold
  • If AP fires contractile force enhanced
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29
Q

Chewing

A

Both a voluntary and involuntary process.

Functions:

  • Mixing food with saliva to lubricate and facilitate swallowing
  • Exposing starches to salivary α-amylase to initiate digestion
  • Reducing size of food particles
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30
Q

Swallowing Reflex

A

Initiated voluntarily then becomes mostly a reflex action.

  1. Initiated when touch receptors of pharynx stimulated by presence of food.
  2. Afferent sensory impulses sent to swallowing center of medulla and lower pons.
  3. Efferent motor neurons transmit impulses to:
    • musculature of the pharynx and upper esophagus via cranial nerves
    • remainder of the esophagus via vagal motor neurons
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31
Q

Phases of Swallowing

A

Divided into 3 phases:

  1. Oral Phase (voluntary process)
    • Tip of tongue seperates food bolus
    • Tongue presses against hard palate then sweeps backwards forcing bolus into pharynx
    • Bolus stimulates touch receptors triggering swallowing reflex
  2. Pharyngeal Phase (takes < 1 sec)
    • Respiration inhibited
    • Nasopharynx closed
      • prevents food entering nasopharynx
      • opens passage for food to pass into pharynx
    • Vocal cords and larynx move forward and upward against epiglottis
      • prevents food from entering trachea
      • opens upper esophageal sphinchter (UES)
    • UES relaxes to receive bolus
    • Contraction of upper constrictor muscles moves food deep into pharynx
    • Peristaltic wave initiated by contraction of pharyngeal superior constrictor muscles
    • Wave moves towards the esophagus forcing bolus through relaxed UES
  3. Esophageal phase (controlled by swallowing center)
    • Once bolus past UES, esophagus contricts by a reflex action
    • Primary peristaltic wave begins below UES
      • Travels entire esophagus in < 10 secs
      • Moves food bolus in front of it
    • If 1° wave insufficient, resulting esophageal distension triggers a secondary peristaltic wave above point of distention
    • Peristaltic waves modulated by input of sensory fibers to CNS and enteric NS
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32
Q

Esophageal Transit

A

Structure

  • Upper 1/3
    • Composed of skeletal muscle
    • Innervated by somatic motor fibers
  • Lower 2/3
    • Composed of smooth muscle
    • Fed by branches vagus nerve
    • Myenteric plexus neurons directly innervate smooth muscle cells

Transit

  • Peristatic wave propels food along esophagus
  • Associated pressure wave moves downward
    • Detected by manometer
  • Relaxation of lower esophageal sphincter (LES) allows food into stomach
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33
Q

Esophagus

Neural Control

A
  • Tonic contraction of LES regulated by intrinsic and extrinsic nerves & hormones.
    • Most of the resting tone of LES mediated by excitatory vagal cholinergic nerves
  • SNS stimulation contracts LES
  • LES relaxes with initiation of peristalsis
    • ​Vagus nerve → enteric nerves → inhibit circular muscles of LES via:
      • neurocrines
      • VIP
      • nitric oxide (NO)
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34
Q

Achalasia

A
  • Failure of LES to completely relax with swallowing and esophageal peristalsis
  • Symptoms:
    • dysphagia
    • regurgitation
    • aspiration pneumonia
  • Treat by stretching or sweakening LES with surgery or drugs
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35
Q

GERD

A
  • Reflux of acidic gastric contents into esophagus
  • Caused by:
    • inadequate closure of LES
    • hiatal hernia which reduces ability of diaphragm to act as additional sphincter
  • Sx include heart burn and regurgitation
  • Sequela:
    • erosions and ulcerations of epithelium
    • esophageal stricture
    • columnar epithelium metaplasia (Barrett’s esophagus)
  • Treatment:
    • PPI
    • hernia repair
    • LES closure
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36
Q

Diffuse Esophageal Spasms

A
  • Disorder of peristalsis
  • Simultaneous contractions of long duration of high amplitude
  • Dysphagia and chest pain
  • Treat with calcium channel blocks
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37
Q

Functions of Saliva

A
  1. Lubricate food
  2. Facilitate speech
  3. Protection against xerostomia (dry mouth), dental carries, and infections
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38
Q

Salivary Components

A
  1. HCO3-
    • maintains basic pH
  2. sIgA against oral flora
  3. Mucins
    • responsible for viscosity
    • most abundant protein in saliva
  4. Lysozyme
    • disrupts bacterial cell walls
  5. Lactoferrin
    • iron-binding protein to inhibit bateria
  6. Salivary α-amylase
    • breaks down starches by cleaving α-1,4-glycosidic bonds
    • destroyed by stomach pH
  7. Lingual lipase
    • hydrolyzes lipids
    • remains active throughout GI tract
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39
Q

Salivary Glands

Names

A

Three pairs of salivary glands:

  1. Parotid
    • mostly serous
    • contains mainly water and salt
  2. Submandibular
    • mixed secretions
  3. Submaxillary / Sublingual
    • mixed secretions
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40
Q

Salivary Gland

Structure

A
  • Salivon: basic unit of a salivary gland
    • Contains:
      • Acinus
        • Serous cells:
          • secrete watery isotonic fluid
          • contains proteins such a α-amylase
        • Mucous cells:
          • secrete mucins
          • gives saliva its viscosity
      • Intercalated duct
      • Striated duct
      • Excretory duct
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41
Q

Saliva Production

Control

A
  • Flow increased by:
    • smell and taste of food
    • mechanical pressure in mouth
    • various reflexes
  • Flow decreased by:
    • stress
    • dehydration
    • sleep
  • Rate of secretion proportional to glandular blood flow.
  • Blood flow under ANS control:
    • Parasympathetic
      • Leads to vasodilation
        • Ach → M3 muscarinic
        • Substance P
        • VIP
      • Increases fluid secretion by acinar cells
      • Increases synthesis of salivary α-amylase and to lesser extent mucins
      • Increases transport in striated and excretory duct cells
      • Net result is increased production of watery saliva rich in electrolytes and salivary α-amylase.
    • Sympathetic
      • Norepi → β-adrenergic receptors
      • Increases salivary flow by stimulating contraction of striated duct cells
      • Results in slightly increased production of viscous saliva richer in proteins and mucins
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42
Q

Salivary Acinar Secretion

A

Iso-osmotic to plasma.

  • Basolateral
    • Na/K-ATPase
      • 3 Na+ out to interstitium
      • 2 K+ into cell
    • Na/H exchanger
      • Na+ into cell
      • H+ out to interstitium
    • Na/K/Cl cotransporter
      • Na+ into cell
      • K+ into cell
      • 2 Cl- into cell
  • Apical
    • Cl/HCO3 cotransporter
      • HCO3- out to lumen
      • Cl- out to lumen
  • Paracellular
    • Cl/HCO3 cotransporter established transepithelial potential with lumen negative
    • Favors Na+ movement into lumen via paracellular pathway
  • Intracellular
    • Carbonic anhydrase
      • HCO3- and H+ generated from CO2
  • H2O moves into lumen due to osmotic forces
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43
Q

Ductal Modification

of

Saliva Composition

A

Electrolyte content altered as saliva travels down intercalated and striated ducts.

Cells relatively water-impermeant.

Na+ and Cl- absorbed.

K+ and HCO3- secreted.

Net movement of salt without water produces hypotonic saliva.

  • Basolateral
    • Na/K-ATPase
      • 3 Na+ out to interstitium
      • 2 K+ into cell
    • Na/H exchanger
      • H+ out to interstitium
      • Na+ into cell
    • Na/HCO3 cotransporter
      • Na+ out to interstitium
      • 2 HCO3- into cell
    • Cl- channel
      • Cl- out to interstitium
  • Apical
    • Na/H exchanger
      • H+ out to lumen
      • Na+ into cell
    • Epithelial Na+ channel (ENaC)
      • Na+ into cell
    • Cl/HCO3 exchanger
      • HCO3- out to lumen
      • Cl- into cell
    • CFTR Cl- channel
      • Cl- out to lumen
    • H/K exchanger
      • K+ out to lumen
      • H+ into cell
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44
Q

Effect of Rate

Saliva Composition

A

The slower the movement of saliva through the duct system the longer the time for electrolyte exchange.

  • Inc. secretion rate ⇒ dec. Na+ and Cl- absorption & dec. K+ excretion
  • Inc. rate of secretion ⇒ inc. HCO3- levels
    • Due to inc. secretion by acinar cells
    • Ensures saliva remains slightly alkaline
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45
Q

Neural Modification

of

Saliva Composition

A

Acinar Cells

Apical Cl- channels & Basolateral K+ channels

Increased by:

Ach via M3 receptors

Norepi via α-adrenergic receptors

Substance P via NK-1 receptors

Ductal Cells

Cl- excretion by CFTR increased by Norepi via β-adrendergic receptors

Na+ and Cl- absorption decreased by Ach via M3 receptors

Na+ and (indirectly) Cl- absorption increased by aldosterone through ENaC activity.

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46
Q

Stomach

Anatomical Regions

A

Four anatomical regions:

  1. Cardia
    • Where esophageal contents
  2. Fundus
    • Forms the upper curved region
  3. Corpus (body)
    • Main region
  4. Pylorus
    • Lower section
    • Facilitates emptying of gastric contents to duodenum
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47
Q

Stomach

Functional Motor Regions

A

Consists of two functional regions:

  1. Gastric reservoir
    • Fundus and top 1/3 of corpus
    • Muscles maintain a continuous tone
    • No phasic contractions
  2. Antral pump
    • Distal 2/3 of corpus, antrum, and pylorus
    • Distal antrum undergoes phasic contractions
      • Breaks up food increasing SA and aiding digestion
      • Provides propulsive force to move contents into gastroduodenal junction
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48
Q

Stomach Structure

A
  • Three layers of smooth muscle
    • outer longitudinal layer with tonic smooth muscle
    • middle circular layer with phasic smooth muscle
    • inner layer formed by two bands of smooth muscle:
      • radiates from LES
      • fuse with circular muscle at caudal area
  • Layers of muscularis externa
    • thin in the fundus and body
    • become thicker in the antrum
  • Mucosa
    • Contains various secretory cells
      • Corpus
        • Parietal cells
          • acid
          • intrinsic factor
        • Chief cells
          • pepsinogen
      • Antrum
        • Chief cells
        • Various endocrine cells
          • G & D cells
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49
Q

Stomach Innervation

A
  • Parasympathetic
    • Vagus nerve
    • Leads to motility and secretion
  • Sympathetic
    • Celiac plexus
    • Inhibits digestive functions
  • Sensory fibers
    • Some leave via vagus and other with celiac plexus
    • Some afferent links between sensory receptors and intramural plexuses
    • Relay information about:
      • intragastric pressure
      • gastric distention
      • pH
      • pain
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50
Q

Responses to Gastric Filling

A
  1. Receptive relaxation
    • Act of swallowing activates a vagovagal reflex
    • Relaxes LES and fundus
    • Anticipates food entering stomach
  2. Adaptive relaxation (or gastric accommodation)
    • Distention of gastric reservoir by food activates a vagovagal reflex
    • Large increase in stomach volume with little increase in intraluminal pressure
    • Lost after vagotomy
51
Q

Migrating Motor Complex

(MCC)

A

a.k.a. migrating myoelectric complex

  • Occurs during fasted state
  • Stomach quiescent for 75 - 90 mins
  • Followed by vigours contractions in the antrum lasting 5-10
  • Pylorus is relaxed
  • Cyclical activity sweeps from stomach to terminal ileum
  • Functions to move undigested contents from stomach → small intestine → colon
  • Maintains low bacterial count in upper intestine
  • MMC in stomach terminated by eating → fed pattern emerges
  • Initiated by Motilin
  • Propagated by enteric NS
52
Q

Fed Pattern

Gastric Contractions

A
  • Eating terminates MMCs in stomach
  • In fed state, gastric contractions ~ 3/min
  • Slow waves driven by ICC pacemakers
    • Propagates towards pylorus
    • Gastric smooth muscle contractions occur when threshold crossed
    • Body has slow waves without AP’s
    • AP in atrum occurs during plateau phase of slow wave
  • Contractions in atrum much stronger than in body
  • Frequency and amplitude of slow waves modulated by neural and hormonal input:
    • Ach and gastrin stimulate contractions
    • Norepi diminishes contractions
53
Q

Mixing and Emptying

Gastric Contents

A

Liquids readily move from stomach into duodenum.

Solids must be reduced to ~ 2 mm before moving to small intestine.

  • Propulsion
    • gastric contractions originate in the middle of the body
    • travel towards pylorus increasing in force and velocity
  • Grinding
    • majority of mixing activity occurs in the antrum
    • as peristaltic wave → antrum, pyloric sphincter shuts
    • small amount of chyme enters duodenum
  • Retropulsion
    • remaining chyme propelled back to fundus and body for more mixing
    • cycle repeats until particles ~ 2mm
54
Q

Gastroduodenal Junction

A
  • Functions of gastroduodenal Junction:
    • regulation of gastric emptying
    • prevention of regurgitation
  • Pylorus seperates antrum and proximal duodenum
    • Neural control
      • Sympathetic input increases pyloric constriction
      • Parasympathetic (vagal) input mixed:
        • excitatory (constriction) ⇒ cholinergic
        • inhibitory (relexation) ⇒ VIP and NO
    • Hormonal control
      • Promote pyloric constriction ⇒ slow gastric emptying
        • CCK
        • gastrin
        • gastric inhibitory peptide (GIP)
        • secretin
  • Proximal Duodenum
    • Influenced by slow waves of:
      • stomach (3-5/min)
      • duodenum (11-13/min)
    • Contracts irregularly
  • When antrum contracts, proximal duodenum often relaxed.
55
Q

Gastric Emptying

Regulation

A

~ 3 hrs to empty 1,500 ml

Tightly controlled by neural and hormonal mechanisms.

  • Sensory receptors in duodenal and jejunal mucosa sense:
    • osmotic pressure
    • pH
    • fats and fat digestion products
    • peptides
    • amino acids
  • Distention promotes emptying.
    • The greater the ingested volume, the faster the rate of emptying.
  • Relative rate based on dominant nutrient class:
    liquids > carbs > proteins > fats
    • Amino acids and proteins
      • Stimulate gastrin from G cells in antrum and duodenum
        • Inc. antral contractions
        • Inc. pyloric contractions
        • Net dec. in gastric emptying
      • Stimulates GIP and CKK secretions
        • Inhibits gastric emptying
    • Fats and monoglycerides in jejunum
      • Stimulates CCK and GIP
      • Both slow gastric emptying
  • Hypertonic solutions slow gastric emptying
    • Chyme becomes more hypertonic in duodenum
      • Added digestive enzymes
      • Increased # particles
  • Acid slows gastric emptying
    • Secretin released d/t acid in duodenum
      • Inhibits antral contractions
      • Stimulates pyloric sphincter contraction
56
Q

Enterogastrones

A

Hormones released from the intestine which affects gastric secretions.

57
Q

Vomiting

A

Expulsion of gastric/duodenal contents via the mouth.

Reflex behavior controlled by vomiting center in medulla.

Triggered by gastric distention, throat tickle, GU injury, dissiness.

  1. Stimulus sent to vomiting center.
  2. May begin with wave of reverse peristalsis, duodenum → stomach.
    • Severe obstruction primary stimulus for this
  3. Pylorus and stomach relax to accomodate contents.
  4. Forced expiration occurs against a closed glottis.
    • Dec. intrathoracic pressure
    • Inc. intra-abdominal pressure
  5. Strong contration of abdominal muscles
    • Further inc. intra-abdominal pressure
    • Forces gastric contents into esophagus
      • Accompanies relaxation of UES
  6. LES relaxes while pylorus and antrum contract.
  7. Gastric contents ⇒ esophagus, with relaxation of UES.
  8. Emesis

Retching

  • Gastric contents forced into esophagus but not pharynx
    • Because UES closed
  • Respiratory and abdominal muscles relax
  • Secondary peristalis returns contents to stomach
  • Typically, series of retches precedes vomiting.
58
Q

Gastric

HCl

A
  • kills microorganisms
  • cleaves pepsinogen → pepsin
  • maintains low pH needed for pepsin activity
  • secreted by parietal cells
59
Q

Pepsins

A
  • secreted by chief cells as pepsinogen precursor
  • activated by acid in stomach
  • digests proteins and peptides
60
Q

Intrinsic Factor

A
  • secreted by parietal cells
  • binds Vit B12 allowing absorption in the ileum
61
Q

Mucous and Bicarbonate

A
  • Secreted by mucous neck cells → serous thinner mucous
  • Secreted by surface epitheliam cells → thicker mucous
  • protects stomach epithelium from damage
62
Q

Gastric Juice

A
  • mixture of secretions from gastric epithelial cells and glands
    • Non-parietal cells
      • Secretion constant and low volume
      • Mostly Na+ and Cl-
      • K+, and HCO3- at plasma concentration
    • Parietal cells
      • Secrete 150 mM HCl solution with 10-20 mL KCl
        • Secrete acid and Cl- against gradient
  • ionic composion depends on rate of secretion
    • slow → hypotonic
      • primarily NaCl with pH ~ 2
    • fast → almost isotonic
      • Na+ decreases
      • H+ increases
    • K+ always higher than plasma → prolonged vomiting = hypokalemia
    • as rate increases parietal cell compnent increases while non-parietal stays constant → approaches pure parietal secretion
63
Q

Parietal Cell

A

Secretes acid against 106 concentration gradient.

  • Intracellular
    • CO2 converted to H+ and HCO3- by carbonic anhydrase
  • Apical
    • H+/K+ exchanger
      • H+ into lumen while K+ enters cell
      • main acid transporter
      • target for PPIs
    • Cl- channel
      • Allows Cl- to move down gradient into lumen
      • Combined with H+ to form HCl
    • K+ channel
      • K+ out on both apical and basolateral membranes
      • Luminal K+ recycled to drive movement of H+ into lumen
  • Basolateral
    • Na/K-ATPase
      • Moves Na out and K in
      • Sets up intracellular K gradient
    • Cl/HCO3 exchanger
      • Bicarb into interstitium
        • Causes alkaline venous blood
      • Cl- into cell
    • K+ channel
      • K+ out on both
64
Q

Control of Acid Secretion

Parietal Cell

A
  • Directly stimulated by:
    • Ach
      • Vagus nerve → M3 muscarinic → Ca++ → PKC
    • Gastrin
      • G cells → CCKB receptors → Ca++ → PKC
        • In response to
          • PNS stimulation
          • amino acids and peptides in chyme
    • Histamine
      • Enterochromaffin-like (ECL) cells → H2 receptors → Adenylate cyclase → PKA
        • In response to Ach & gastrin binding ECL cells
      • Receptor target for H2 blockers
    • Synergistic response ⇒ potentiation
  • Inhibited by:
    • Somatostatin
    • Prostaglandins (E and I)
    • Epidermal growth factor (EGF)
    • All 3 act through inhibit of adenylyl cyclase → dec. cAMP
65
Q

Gastric Acid Secretion Phases

A
  1. Cephalic phase
    • Triggered by food
    • Vagovagal reflex to parietal and G cells
    • ~40% of total gastric secretion
  2. Gastric phase
    • Triggered by:
      • stomach distention
        • mechanoreceptors → enteric & CNS → Ach → direct stimulation of parietal cells (acid) and G cells (gastrin)
        • Gastrin stimulates acid release
      • presence of amino acids and peptides
      • other chemicals like alcohol and caffeine
      • ~50% of gastric secretions
  3. Intestinal phase
    1. Triggered by protein digestion products in chyme in duodenum
      1. Duodenal distention triggers vagovagal reflex → stimulates parietal and G cells
      2. Peptides and AA stimulate G cells of duodenum and proximal jejunum → Gastrin
        1. Also stimulates duodenum to release entero-oxyntin → stimulates acid secretion
    2. Inhibited by acid, fatty acids, monoglycerides, hypertonic chyme in duodenum and proximal jejunum
    3. Stimulated with chyme pH > 3
66
Q

Pepsin Secretion

A

Stimulated by:

  • PNS → vagal stimulation during cephalic and gastric phases → Ach → chief cells → pensinogen
  • Acid → enteric NS → local cholinergic reflex → Chief cells → pepsinogen
    • Secretion increased when luminal pH low
  • Duodenal mucosa → Secretin and CCK → pepsinogen
67
Q

Mucous and Bicarb

Secretion

A
  • Soluble mucous
    • PNS → vagus nerve → Ach → mucous neck cells → soluble mucous
  • Insoluble mucous and HCO3-
    • Secreted by surface epithelial cells
    • In response to chemical or physical irritation
    • Insoluble mucous traps dead cells and bicarb
68
Q

Small Intestine

Structure

A
  • Villi increase surface area
    • Epithelial cells and globlet cells
    • Capillaries and lacteals
  • Crypts of Lieberkuhn
    • openings at base of villi
    • mostly in duodenum and jejunum
    • secrete salts and water
  • Goblet cells secrete mucous
  • Paneth cells secrete defensins
69
Q

Small Intestine

Contractility

A
  1. Peristaltic contractions
    • vectoral movement
    • propels chyme
    • slow waves generated by ICCs control contractions
    • duodenal contractions follow stomach contractions
  2. Segmental contractions
    • most common movement
    • small sections rhythmically contract and relax
    • mix chyme with secretions
  3. Codeine and opiates inhibit contractions
70
Q

Small Intestine

Electrical Activity

A
  • MMCs during fasted state for housekeeping
  • Slow waves generated by ICCs
    • Limited to small areas
    • Can have APs superimposed
      • responsible for segmentation and peristaltic contractions
  • Smooth muscle cell excitability influiced by:
    • direct effects from enteric NS
    • inditect effects from CNS via enteric NS and ICCs
      • PNS increases excitability
      • SNS decreases
71
Q

Law of the Intestine

A

When a material placed in the small intestine, it will contract behind it and relax ahead of it.

Responsible for movement of chyme in proper direction.

72
Q

Intestinointestinal Reflex

A

Overdistension of one segment of the intestine relaxes smooth msucle in the rest of the intestine.

Protects from potential reupture.

Does not faciliate movement.

73
Q

Gastroileal Reflex

A

Elevated stomach activity increases movement of chyme from the terminal ileum into the colon through the ilealcecal sphincter.

74
Q

Brunner’s Glands

A
  • Found in the beginning of the duodenum between pylorus and sphincter of Oddi
  • Secretes HCO3- and mucus
  • Protects epithelial cells from acid in chyme
75
Q

Crypts of Lieberkuhn

A
  • Epithelial cells secrete isotonic fluid
    • Up to 1.8 L/day
  • Keeps chyme in aqueous solution
  • Several transporters involved:
    • Basolateral
      • Na/K-ATPase
        • sets up Na+ gradient
      • NKCC1 cotransporter
        • Na+, K+, and 2 Cl- moved into cell
        • Uses Na+ gradient
    • Apical
      • CFTR Cl- channel
        • Cl- into lumen
        • Activity increased by secretagogues
          • Secretin and VIP → cAMP → PKA → phosphorylates and opens CFTR
    • Cl- movement increases luminal negatvity
    • Na+​ moves into lumen via paracellular pathways
    • Water follows.
76
Q

Incretins

A

Hormones released from the gut that increase insulin secretion in a glucose-dependent manner.

Released in response to glucose in the lumen of small intestine.

Act on β-cells of the endocrine pancreas to stimulate insulin release.

  • Gastric inhibitory peptide (GIP)
    • Secreted by K cells in duodenum and jejunum
  • Glucagon-like intestinal peptide (GLP-1)
    • Secreted by L cells in ileum and colon
77
Q

Exocrine Pancreas

A
  • Secretion of pancreatic juice
    • Aids in digestion
    • Composed of water, salts, and enzymes
      • HCO3 neutralizes stomach HCl
      • Enzymes degrade carbs, proteins, and lipids
  • Secretin stimulates bicarb secretion
    • released in response to acid in chyme
  • CCK stimuates digestive enzyme secretion
    • released in response to protein and fat in chyme
78
Q

Pancreas

Structure and Innervation

A

Structure

  • Pancreatic acinar cells
    • specialized for protein secretion
  • Ductal columnar epithelial cells
    • specific membrane transporters
      • bicarb excretion

Innervation

  • PNS
    • innervated by branches of the vagus nerve
    • synapse with neurons in pancreas
    • use Ach
    • directly stimulates pancreatic juice secretion
  • SNS innervate pancreatic blood vessels
    • activation → vasoconstriction
    • indirectly decreases secretion
    • no direct sympathetic effect on secretions
79
Q

Pancreatic Juice

Aqueous Component

A

Secreted by ductal columnar epithelial cells.

  • Contains entirely water and salts
  • Initially hypertonic but water during duct movement making isotonic
  • Na+ and K+ concentrations similar to plasma
  • HCO3- much higher than plasma
    • concentration increases as rate of secretion increases
  • Cl- concentration reciprocal to bicarb
    • when bicarb high Cl low and vice versa
80
Q

Pancreatic Bicarb Secretion

A
  • Sources:
    • made by carbonic anhydrase
    • transported into cell from basolateral membrane by Na+/HCO3- co-transporter
  • Ductal Cell transporters
    • Basolateral
      • Na+/K+-ATPase sets up gradient
      • Na+/HCO3- co-transporter brings in bicarb
      • Na+/H+ counter transporter and H+ pump
        • removes H+ generated by carbonic anhydrase
        • favors splitting of water needed for bicarb production
    • Apical
      • CFTR Cl- channel
        • moves Cl- into lumen
          • Secretin ⇒ cAMP ⇒ PKA ⇒ activates CFTR
      • Cl-/HCO3- exchanger
        • uses Cl- gradient
        • exchanges luminal Cl- for HCO3-
    • Na+ and water follows Cl-/HCO3- into lumen via paracellular path
  • Ach ⇒ Ca++ ⇒ Ca++-and-calmodulin dependent protein kinase II (CaMK II) ⇒ increases HCO3- secretion via unknown mech
81
Q

Pancreatic Juice

Enzyme Component

A

Released from the pancreatic acinar cells.

Isotonic and similar ion concentration to plasma.

Exocytose Zymogen granules into lumen when stimulated

  • Proteases
    • Trypsinogen
      • Cleaved by enterokinase in duodenum
      • Trypsin cleaves other zymogens
      • Trypsin inhibitor secreted from acini to inhibit prematurely formed trypsin
    • Chymotrypsinogen
    • Procarboxypeptidase
  • Pancreatic α-amylase
    • Degrades starches
    • Secreted in active form
  • Lipase
    • Requires co-lipase coenzyme to function
    • Fat degradation
  • RNAse & DNAse
    • degrade nucleic acids
82
Q

Pancreatic Enzyme Secretion

Regulation

A

Secretin and CCK secreted by duodenal mucosa.

  • Ach and CCK ⇒ Ca++ mechanism
  • Secretin and VIP ⇒ cAMP-mediated
  • PNS vagal stimulation activates secretion of pancreatic juices
  • SNS stimulation decreases in blood flow
    • indirectly inhibits pancreatic secretion
83
Q

Pancreatic Secretion

Phases

A
  1. Cephalic Phase
    • Triggered by food
    • Vagus stimulation via muscarinic Ach receptors on acinar cells
    • Volume of pancreatic juice secreted low
    • Predominantly enzymatic
  2. Gastric Phase
    • Triggered by food entering stomach
    • Vagovagal reflex starts in stomach
      • Induces pancreatic secretion
    • Gastrin released by stomach in response to AA
      • Activates CCK receptors on pancreatic acinar cells
      • Stimulates pancreatic secretion
    • Predominant effect on enzyme secretion
  3. Intestinal Phase
    • Vagovagal reflexes stimulate pancraetic secretion
    • Acid in chyme stimuates Secretin
      • Secretin stimulates production of large volumes of pancreatic juice
      • Low enzyme concentration
      • High bicarb
    • AA and peptides in chyme in duodenum
      • Stimulate release of CCK from duodenal mucosa
      • CCK stimulates pancreatic enzyme release
    • Fatty acids and monoacylglycerols in duodenum
      • Stimulates CCK release
      • CCK stimulates pancreatic enzyme release
    • CCK and secretin work synergistically
84
Q

Carbohydrate

Digestion

A
  • Starch (glucose, α-1,4- linkages with α-1,6 branches)
    • main dietary carbohydrate
    • salivary α-amylase in mouth
      • breaks α-1,4-linkages only
    • pancreatic α-amylase in duodenum
      • glucose polymers
      • limit dextrin
    • oligosaccharidases
      • membrane bound at brush border
      • break down into glucose monomers
      • α-dextrinase for limit dextrin
      • glucoamylase (maltase) for glucose polymers
  • Lactose (glucose-galactose)
    • Lactase breaks down to monomers
  • Sucrose (glucose-fructose)
    • Sucrase breaks into monomers
85
Q

Carbohydrate

Absorption

A
  • Greatest absorption in duodenum
    • Decreasing as chyme travels down small intestine
  • All mono and di-sacch. absorbed in small intestine
  • 80-90% of start absorbed
    • remainder to colon where degraded by bacteria
  • Na+-dependent glucose transporter (SGLT1)
    • glucose and galactose into cell
    • secondary active transport
  • GLUT 5
    • fructose into cell
    • facilitated transporter
  • GLUT 2
    • facilitated transporter
    • move all monosaccharides out of basolateral membrane
86
Q

Lactose Intolerance

A
  • Deficiency of lactase after childhood
    • normal occurance
  • Lactose not degraded
  • Enters colon where degraded by bacteria
    • Causes gas and diarrhea
87
Q

Congentital Lactose Intolerance

A

Complete loss of lactase at all life stages.

Rare.

88
Q

Glucose-galactose Malabsorption

A
  • Due to defect in SGLT1
  • Cannot absorb glucose or galactose
  • All carbs from fructose
  • Avoid starch, sucrose, and lactose
89
Q

Protein

Digestion

A
  • Pancreactic Proteases
    • Trypsin
      • Activated by enterokinase
      • cleaves other inactive enzymes
    • Chymotrypsin
    • Carboxypeptidases
  • In duodenum:
    • Proteases degrade proteins into peptides containing 3-8 AA and free AA
  • On brush border:
    • Membrane bound oligopeptidases and peptidases
      • Cleave most small peptides to free AA
  • Almost all protein cleaved to free AA, di- and tri-peptides in small intestine lumen
90
Q

Protein

Absorption

A
  • Greatest amount in duodenum
    • Decreases as chyme moves down small intestine
  • Na+/amino acid cotransporters
    • primary free AA transporter
    • uses Na+ gradient
  • H+/peptide cotransporter (PepT1)
    • transport di- and tri-peptides
    • uses H+ gradient set up by Na+/H+exchanger on apical membrane
  • Inside the cell
    • di- and tri-peptides broken down into free AA by peptidases
  • Free AA transported into blood by basolateral AA transporters
    • two Na+ dependent
    • three Na+ independent
    • each has specificity towards specific types of AA
91
Q

Intact Protein

Absorption

A
  • Small amount of protein absorbed by phagocytosis
  • important during first 6 months post-natal
  • aids in transfer of immunity
  • after 6 months, decreases to very low levels
  • primarily important for antigen uptake and clearance
92
Q

Water

Absorption

A
  • Ingest 2-2.5 L/day
  • Secrete ~ 7 L/day into GI tract
  • Only ~ 0.1 L excreted in feces
  • Absorb almost 9 L/day
  • no net water absorption in duodenum
  • most water absorbed in jejunum and ileum
  • ~ 2 L/day reaches colon
    • 1.9 L reabsorbed
93
Q

Intestinal

Na+ Absorption

A
  • occurs throughout small intestine
    • little net absorption in duodenum
    • most occurs in jejunum and ileum
  • Basolateral N+/K+-ATPase
    • sets up gradient for other transport systems
  • Most Na reabsorbed by sugar or AA linked co-transport systems
  • Na+/H+ exchanger on apical membrane
  • Amiloride-sensitive Na+ channels (ENaC)
    • on apical membrane mainly in colon
94
Q

Intestinal

Cl- Absorption

A
  • Little net absorption in duodenum due to excretions
  • Cl- reabsorbed via paracellular pathway in jejunum and ileum
    • Direction of movement dependent on electrochemical gradient
  • Exchanged for bicarb by Cl-/HCO3- exchanger
95
Q

Intestinal

HCO3- Absorption

A
  • In duodenum and jejunum:
    • HCO3- reacts with H+ to form H2CO3
      • H+ pumped into lumen by Na+/H+ exchanger
    • H2CO3 broken down by carbonic anhydrase to CO2 and H2O
    • CO2 diffuses across epithelial cell
    • Net absorption of bicarbonate
  • In ileum:
    • basolateral Na+/K+-ATPase
      • ​sets up gradient
    • basolateral Na+/HCO3- co-transporter
      • ​brings HCO3- into cell
    • apical Cl-/HCO3- counter-transporter
      • net excretion of HCO3-
      • net absorption of Cl-
96
Q

Intestinal

K+ Absorption

A
  • Small intestine
    • Luminal [K+] progressively increases
      • Due to movement of NacL, sugar, and AA from lumen
    • When [K+] becomes high enough it moves via paracellular path
      • Mostly through solvent drag by water
    • Net absorption of K+ occurs
  • No active transport of K+
97
Q

Intestinal

Ca2+ Absorption

A

Absorbed by both passive and active processes.

  • Passive paracellular transport
    • Occurs throughout small intestine
  • Active Ca2+ transport
    • Only in duodenum
    • Ca2+ moves down electrochemical gradient through Ca2+ channel
    • Inside cell:
      • Binds to calbindin
      • take up by intracellular vesicles
    • Bound Ca2+ excreted across basolateral membrane by:
      • Ca2+-ATPase
      • N+/Ca2+-exchanger
  • Active process regulated by Vit D (and indirectly by PTH)
    • Stimulates synthesis of calbindin, Ca2+-channels, and Ca2+-ATPases
    • Total Ca2+ absorption low in absence of Vit D
98
Q

Ca2+ Deficiency

A

Lack of Ca2+ absorption can result in:

rickets in children

osteomalacia in adults

Marked by softening of bones.

99
Q

Intestinal

Iron Absorption

A
  • Dietary iron in two forms:
    • Heme iron
    • Non-heme iron
    • Both poorly absorbed (10-20% dietary intake)
  • Heme Iron:
    • always in ferrous form
    • taken into cell by unknown mechanism
    • inside cell, heme oxygenase:
      • splits heme
      • oxidizes Fe2+to Fe3+
    • Fe3+ treated like non-heme iron
  • Non-heme iron:
    • Ferric (Fe3+) or Ferrous (Fe2+) forms
      • Only absorbed in ferrous form
    • Dcytb
      • iron reductase on brush border
      • reduces ferric to ferrous form
    • DMT
      • H+/Fe2+- cotransporter
      • Moves Fe2+ into cell
    • Fe2+ binds mobilferrin inside cell
    • moved to basolateral membrane
    • Ferroportin (IREG1) transport out of cell
    • Oxidized to Fe3+ by ferroxidase-hephaestin
    • Binds to transferrin for transport through blood
100
Q

Hemochromatosis

A
  • Disorder of excess iron absorption
  • Iron can accumulate in tissues causing damage
    • cirrhosis
    • hepatomas
  • Defect appears to involve hepcidin
    • normally downregulates DMT expression
101
Q

Bile

Overview

A
  • Primary secretion (bile)
    • Secreted by hepatocytes at the end of ducts
    • Contains bile acids, cholesterol, and PL
    • Stimulated by CCK
  • Ductal cells secrete fluid with ions and bicar
    • Stimulated by secretin
  • Stored and concentrated in the gallbladder
    • Post-prandial CCK stimulates contration and excretion
  • Bile acids emsulsifies fat in duodenum forming micells
102
Q

Bile Concentration

A
  • Concentrated x20 in gallbladder
  • Standing Osmotic Gradient Hypothesis
    • Transporters set up an osmotic gradient that drives water movement​
  • Apical Na+/H+ counter-transporter moves Na+ into cell
  • Basolateral Na+/K+-ATPase moves Na+ into interstitium
  • Basolateral K+ channel acts as K+ shuttle for Na+/K+-ATPase
  • Apical Cl-/HCO3- exchanger moves HCO3- into lumen
    • HCO3- neutralizes secreted acids
    • Cl- enters cell
  • Basolateral Cl- channel moves Cl- into insterstitium
  • Net Na+ and Cl- movement into insterstitium establishes an osmotic gradient
  • Water follows Na+ and Cl- into paracellular and instertitial space via aquaporins
103
Q

Gallbladder Emptying

A
  • During cephalic and gastric phases:
    • Gallbladder contracts
    • Sphincter of Oddi relaxes
    • Allows small amount of contents into duodenum
    • Stimulated by:
      • Vagus nerve
      • Gastrin released from stomach
  • During intestinal phase:
    • CCK released from duodenal cells
      • Strong gallbladder contractions
      • Complete relaxation of the Sphincter of Oddi
    • Allows gallbladder to completely empty
104
Q

Enterohepatic Recirculation

A
  • Bile acids reabsorbed in the terminal ileum:
    • Cross apical membrane via Na+/bile salt transporter (ASBT)
    • Leave basolateral membrane via Na+-independent organic solute transporter
    • Transported in the blood to liver by Na+-dependent process
    • Bound to bile acid-binding proteins
    • Secreted into canaliculi
  • Can be recycled > 5 times with fatty mean
105
Q

Micelle Formation

A
  • Bile acids form micelles when concentration reaches critical micellar concentration (CMC)
  • Phospholipid/cholesterol vesicles from liver mix with micelles to form mixed micelles
  • Monoacylglycerol and FA from fat breakdown remain in mixed micelles until absorption
  • If cholesterol levels too high system supersaturated
    • Can form gallstones blocking bile duct
106
Q

Bile Pigments

A
  • Heme catabolized to bilirubin
  • Accumulates in blood ⇒ liver
  • Excreted in bile afte conjugation with glucuronates
107
Q

Bile

Aqueous Components

A
  • Cholangiocytes (bile duct cells) secrete aqueous solution
    • isotonic
    • higher HCO3-
    • lower Cl-
  • Stimulated by secretin ⇒ cAMP ⇒ PKA ⇒ phosphorylation of CFTR Cl- channels
    • initiates Cl- recycling and Cl-/HCO3- exchange
  • Also stimulated by:
    • glucagon
    • VIP
  • Inhibited by:
    • Somatostatin
108
Q

Digestion of Lipids

A

Occurs in the Duodenum and Jejunum.

  • Mixed micelles increase SA of exposed lipids
  • Pancreatic lipases
    • requires colipase to remove inhibition by bile salts
    • ​break down TAG at water-micelle interface:
      • two fatty acids
      • monoacyl glycerol
  • Cholesterol ester hydrolase
    • pancreatic enzyme
    • degrades cholesterol esters to:
      • cholesterol
      • fatty acid
    • products remain in micelles until absorbed into epithelial cells
  • Phospholipase-A2
    • pancreatic enzyme
    • degrades phospholipids to:
      • fatty acids
      • lysolipid (PL with only one FA)
109
Q

Lipid Digestion Products

Absorption

A
  • Micelles composed of monoacylglyerol, FA, lysolipids, and cholesterol.
  • Pass through unstirred layer at surface of epithelial cells
    • Na/H exchanger makes layer acidic
    • Causes FA to be protonated ⇒ uncharged
    • Movement through layer aided by:
      • segmentation contractions
      • contraction of muscularis mucosa
  • Hypdrophobic digestion products diffuse through apical membrane into cell.
  • FA transported to ER by fatty acid binding proteins (FABP)
  • Glycerol diffuses out into blood
110
Q

Intracellular Lipid Processing

A
  • Lipids move to ER bound to FABPs
  • Converted back to complex lipids:
    • Monoacylglycerol + FA = TAG
    • Lysolipid + FA = phospholipids
    • Cholesterol + FA = cholesterol ester
  • In golgi, new lipids combine with apolipoproteins forming chylomicrons
    • Abetalipoproteinemia ⇒ inability to form chylomicrons
      • Steatorrhea
  • Secreted into lacteals ⇒ lymph ⇒ thoracic duct ⇒ blood
111
Q

Large Intestine

Structure

A
  • Starts at ileocecal sphincter
    • Distension of distal ileum ⇒ peristalsis ⇒ sphincter relaxation ⇒ movement of chyme into proximal colon
    • Sphincter closes as proximal colon becomes distended
  • Smooth muscle
    • primarily circular smooth muscle
    • longitudinal smooth muscle in 3 band ⇒ taenia coli
  • Anal canal
    • end of the colon
    • closed by:
      • internal anal sphincter ⇒ smooth muscle
      • external anal sphincter ⇒ skeletal
        • innervated by somatic motor fibers from pudendal nerve
  • ​​​Colonic contractions
    • Mix chyme
    • Moves it along epithelial surface very slowly
  • Mass movement
    • Occurs 1-3 times / day
    • Colonic contents move a significant distance
    • Segments remain contracted for several minutes
112
Q

Cecum and Proximal Colon

Motility

A
  • In proximal colon:
    • contractions segmental ⇒ Haustra
      process ⇒​ Haustration
      • mixes chyme
      • little vectoral motion
    • slows movement of chyme so salt and water can be reabsorbed
113
Q

Central and Distal Colon

Motility

A
  • Mass movements move semi-solid feces to mid-colon
  • Colonic contractions continue to mix feces
  • Additional mass movements push feces towards end of the colon and into rectum
114
Q

Colonic Motility

Regulation

A
  • Direct control of colonic contractions from intramural plexus
    • Stimulatory nerves ⇒​ Ach and substance P
    • Inhibitory nerves ⇒​ VIP and nitric oxide
  • Extrinsic nerves only have indirect effects.
115
Q

Colonic Electrophysiology

A
  • Colonic circular smooth cells rarely produces APs independently
  • Interstitial cells of Cajal (ICCs)
    • near inner border of smooth muscle
    • generates slow waves
    • Enteric NS ⇒​ Ach ⇒​ stimulates ICCs
      • increase length of slow waves
    • longer slow waves cause contraction
  • Second class of ICCs
    • near outer border
    • generates myenteric potential oscillations
      • lower in amplitude
      • higher frequency
    • may produce APs generating contractions
116
Q

Colonocolonic Reflex

A

When one part of the colon is distended, the other parts relax.

Reflex initiated by sympathetic nerve fibers.

117
Q

Gastrocolic Reflex

A

When food enters the stomach, colonic smooth muscle contracts producing a mass movement.

Sometimes of sufficient pressure to produce need to defecate.

118
Q

Defecation

A
  • Mass movement in sigmoid colon fills rectum with feces
  • Triggers a rectosphincteric reflex:
    • relaxes internal anal sphincter
    • constricts external anal sphincter
    • interpreted as urge to defecate
  • Defecation starts with voluntary relaxation of the external anal sphincter
  • Other voluntary actions include:
    • deep breathing to increase abd pressure
    • contracting abnormal wall muscles
    • relaxation of pelvic floor
  • Involves strong contractions of the descending and sigmoid colon
    • Reflex controlled by sacral spinal cord with PNS fibers
119
Q

Colonic

NaCl Absorption

A

Two different mechanisms:

  1. Early or proximal colon
    • Na+/H+ exchanger
    • Cl-/HCO3- exchanger
  2. Distal colon
    • Aldosterone senstitive Na+ channel (ENaC) on apical membrane
      • Produces large transepithelial potential with lumen negative
    • Cl- movement via paracellular path
120
Q

Colonic

K+ secretion

A

Colon is a net secretor of K+.

Occurs over entire length of colon.

  • Passive K+ secretion
    • Responsible for overall net K+​ loss
    • Paracellular path
    • Driven by negative transepithelial potential
      • most negative at distal end of colon
      • passage the greatest there
  • Active K+ ​secretion
    • pump-leak mechanism
    • K+​ crosses basolateral membrane via:
      • Na+/K+​-ATPase
      • Na+/K+/Cl- cotransporter (NKCC1)
    • Intracellular K+​​ uses a K+​ channels to either:
      • be recycled back across basolateral membrane
      • be secreted across apical membrane
    • Whether secretion takes place depends on amount of K+​​ channels on apical membrane
      • Aldosterone and VIP (via cAMP) increases channel density thus secretion
  • Active K+​​ Absorption
    • Only takes place in the distal colon
    • Driven by apical H+/K+​-ATPase
    • K+​ then crosses basolateral membrane by unknown process
121
Q

Colonic

HCO3- and Mucous Secretion

A
  • HCO3- exchanged for Cl-
  • Mucus secreted from goblet cells throughout colonic mucosa
    • Stimulated by mechanical irritation of mucosal surface
122
Q

Stomach Gases

A
  • Mostly nitrogen and oxygen from swallowed air
  • Normally expelled by belching
  • Gases not expelled move into small intestine
  • Borborygmi = sounds produced by movement of gas in stomach antrum & small intestine
123
Q

Small Intestine Gases

A
  • Normally very little gas in small intestine
  • Usually just oxygen and nitrogen from stomach
  • CO2 can build up if reaction between gastric acid and bicarb too rapid
    • Ability to reabsorb gas then exceeded
  • Gases usually make noise
  • Silent abdomen suggestive of intestinal immobility
124
Q

Colonic Gases

A
  • Gases mostly derived from bacterial action
  • Includes:
    • CO2
    • H2
    • odoriferous gases like indole
    • sulfur-containing compounds
  • Worse with carbs or high fiber diet
  • Worse with sudden diet changes
  • Excess gas expelled as flatus

IMS: Physiology (14 decks)

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