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U7 GI Physiology > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

Secretin

A

Source: S cells lining duodenum

Stimulated by acid entering duodenum

Inhibits stomach motility and gastric acid secretion

Stimulates aqueous (bicarb) secretion from pancreas

Stim. gastric chief cells to release pepsinogen

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2
Q

CCK

A

Source: I cells in dueodenum and jejunum

Stimulated by fat and amino acids entering duodenum

Inhibits emptying of stomach

Stimulates enzyme secretion by pancreas (acinar cells) and potentiates aqueous secretion

Causes contraction of gall blabber and relaxation of sphincter of Oddi

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3
Q

Gastrin

A

Sources:

  • G cells of stomach
  • Stimulated by stomach distention
  • Acts to increase acid secretion (parietal cells)
  • Stimulates growth of gastric mucosa
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4
Q

GIP (glucose insulinotropic peptide)

A

Source: duodenum

Stimulated by fat, CHO, amino acid

Inhibits stomach acid motility and secretion

In gallbladder: increases insulin, decreases glucagon

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5
Q

Events during swallowing

A
  1. Pharyngeal phase: Food in pharynx –> sensory from CN IX and X to medulla, efferent impulses sent back
  2. Relaxation of UES (skeletal muscle)
  3. Primary peristaltic wave
  4. Relaxation of LES (smooth mucles) via VIP acting as an inhibitory NT
    - Fails in achalasia (abnormal enteric nerves)
    - Tone not maintained in GERD, stomach acid refluxes back into esophagus
  5. Relaxation of proximal stomach (receptive relaxation)
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6
Q

Stimulation of gastric motility

A
  • Increased parasym via ACh and gastrin

**- **Local distention

  • Atropine (ACh receptor antagonist) alone cannot slow stomach b.c GRP/Gastrin bypass ACh
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7
Q

Inhibition of gastric motility

A
  • Low pH of stomach contents inhibits release of gastrin
  • Feedback from duodenal overload (neural and hormonal)
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8
Q

Stomach emptying

A

Liquids > carbs > proteins > fat

Pyloris is a sphincter that controls rate of empyting

CCK, GIP, secretin slow stomach emptying by increasing contraction of pyloric sphincter

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9
Q

Migrating Myoelectric Complex (MMC)

A
  • Propulsion during fasting, begins in stomach and moves undigested material from stomach –> small intestine –> colon
  • Repeats every 90-120 min during fasting
  • Correlated with high motilin levels (hormone of small intestine)
  • Prevents backflow of bacteria from colon into illeum
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10
Q

Defacation

A
  • Reflex of the CNS
  • Filled rectum –> relaxation of internal anal sphincter and contraction of external anal sphincter –> voluntary relaxation of EAS with propulsive contraction of distal colon = poop!
  • Lack of functional innervation of EAS = involuntary pooping when rectum fills
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11
Q

Salivary secretions

A
  • Parotid gland secretions (25%) - entirely serous, rich in a-amylase
  • Submandibular (70%) and sublingual (5%) gland secretions - mixed (mucus and serous), rich in mucin glycoproteins
  • Under control of parasym - promotes secretion

Fxns: lubrication, protection, digestion

Sjogren syndrome (autoimmune, destroys salivary and lacrimal glands)

Xerostomia (dry mouth)

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12
Q

Myenteric Plexus (Auerbach’s)

A
  • Between longitudinal and circular muscle laters
  • From proximal esophagus to rectum
  • Enhances peristalsis (increases tone, intesity, and velocity of contractions)
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13
Q

Submucosal plexus (Meissner’s)

A
  • Between the circular muscle nad submucosa
  • Small and large intestine
  • Controls local intestinal secretions, absorption, and contraction of submucosal muscle
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14
Q

Types of receptors in the enteric nervous system

A
  1. Mechanoreceptors: sense SM stretch, signals through myenteric plexus to stimulate contractions
  2. Chemoreceptors: sense chemical composition of chyme, control luminal pH during influx of acidic chyme
  3. Osmoreceptors: sense osmolarity of chyme, control amount of chyme entering small intestine and secretions to buffer chyme (don’t want to chyme to exert an osmotic force)
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15
Q

PNS Activation of the Enteric Nervous System

A

Parasym preganglionics (vagus and pelvis nerves) terminate on postganglionic cholinergic/peptidergic neurons in plexuses

  • PNS activation = increased gut motility, relaxation of sphincters, enhanced secretions

Vagovagal reflexes: both afferent and efferent impulses are carried by vagus

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16
Q

PNS Innervation of ENS

A
  • Vagus innervates proximal 2/3 (pharynx –> beginning of distal colon)
  • Pelvic nerves innervate distal 1/3 of colon
  • ACh major NT (some postgang fibers release peptides)
  • Activation promotes digestion and absorption
17
Q

SNS innervation of ENS

A
  • Postganglionic fibers from celiac plexus, hypogastric, superior & inferior mesenteric ganglia
  • NE major NT. Many inhibit excitatory ACh neurons
  • Inhibits/reduces digestion and absorption
18
Q

Interstitial Cells of Cajal

A
  • Pacemakes in the GI tract - generate slow waves
  • In myenteric plexus
  • Contraction of GI muscle wall occurs when AP is generated at the peaks of slow waves (above -40mV) –> stimulated of PNS
19
Q

Order of secretory unit in exocrine pancreas

A

Acinus –> intercalated duct –> intralobular duct –> interlobular duct –> main pancreatic duct

20
Q
A
21
Q

Na+ and HCO3- secretion (aqueous secretion) by pancreatic duct cells

A
  1. Diffusion of CO2 from blood
  2. CO2 dissociates to carbonic acid –> H+ and HCO3-
  3. H+ pumped out through Na+/K+ exchanger or proton pump (removed)
  4. HCO3- also enters via Na+/HCO3- exchanger
  5. HCO3- accumulates, enters lumen through Cl-/HCO3- exchanger (depends on available Cl- in lumen, which depends on opening of apical Cl- channel)

Note: Cl- channel (CFTR) is activated by secretin –> increases cAMP –> opens channel –> bicarb can be secreted. Absent in CF patients, can’t secrete bicard

  • Negative charge of lumen (from Cl-) pulls Na+ in across tight jxns

*ACh and secretin stimulate bicarb secretion

22
Q
A
23
Q

What is the “exchange hypothesis” in pancreatic aqueous secretions?

A
  • Electrolye composition of aqueous secretion is a fxn of the rate of secretion
  • Fast secretion = more bicarb (less time for exchange)
  • Slow secretion = less bicarb, more like plasma
24
Q

What causes cystic fibrosis?

A
  • Defective CTFR channel
  • Cl- isn’t replensihed in lumen, bicarb can’t be secreted by the exchanger
  • Ducts become clogged with thick mucous without the aqueous secretions –> causes dyspnea
25
Q

Regulation of pancreatic secretion

A
  1. Cephalic phase (see/smell food): “priming” effect, vagus stim causes release of pancreatic juices
  2. Gastric phase: stomach distention causes release of gastrin from G cells
  3. Acidic chyme in duodenum stim release of secretin, Fatty/protein secretions stim releease of CCK (both enter blood stream)
  4. Reach pancreas: CCK induces secretion of enzymes, secretion causes secretion of bicarb
26
Q
A
27
Q

Composition and function of bile

A
  • Bile salts (recycled by hepatic circulation, form micelles), bile pigments (bilirubin), cholesterol, neutral fats, phospholipids, electrolyes
  • Fx: emulsify fat (they are amphipathic), facilitate fat/cholesterol absorption, help solubilize cholesterol
  • Secreted into bile cancaliculi –> bile ducts –> hepatic ducts –> common bile duct –> duodenum –> cystic duct –> gall bladder
28
Q

Bile micelles

A
  • Composed of bile salts, lecithin, and cholesterol
  • Formed when bile salts are concentrated
  • Essential for absorption and for removal of waste products

U7 GI Physiology (1 decks)

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