GI, Topnotch Flashcards
Basic layers of the GI tract
1) Mucosa 2) Submucosa 3) Muscularis 4) Serosa
GI Mucosa: Layers
1) Epithelium 2) Lamina propria 3) Muscularis mucosa
GI Mucosa: Layer with blood vessels
Lamina propria
Layer of GIT: Contains glands and blood vessels
Submucosa
GI Muscular layers
ICOL 1) Inner circular 2) Outer longitudinal
GI Muscular layers: Decreases diameter
Inner circular
GI Muscular layers: Shortens segment
Outer longitudinal
GI layer: Layer deficient in esophagus
Serosa
GI Submucosal plexus
Meissner’s plexus
GI Myenteric plexus
Auerbach’s plexus
GI Submucosal plexus, function
Secretion, absorption, contraction
Esophagus: Strongest layer
Mucosa
Small intestine: Strongest layer
Submucosa
Stomach: Muscle layers
1) Inner oblique 2) Middle circular 3) Outer Longitudinal
Myenteric plexus: Mainly excitatory except at (2)
1) Pyloric sphincter 2) Ileocecal valve
PSY innvervation: Esophagus to upper large intestine
Vagus
PSY innvervation: Lower large intestine to anus
Pelvic
Gastrin: Source
G cells in antrum
Gastrin: Inhibited by
1) H+ 2) Somatostatin
Gastrin: Action
1) Increases H+ 2) Stimulates growth of gastric mucosa
Gastrin: Location of receptors
1) Parietal cells 2) Enterochromaffin cells
Secretin: Source
S cells in duodenum
Secretin: Stimulus
1) H+ 2) Fatty acids
Secretin: Action
1) Inc pancreatic bicarbonate 2) Inc biliary bicarbonate 3) Decrease effect of gastrin
Cholecystokinin: Source
I cells in duodenum and jejunum
Cholecystokinin: Stimulus
1) Monoglycerides and fatty acids 2) Peptides and amino acids
Cholecystokinin: Action
1) Gallbladder contraction 2) Sphincter of Oddi relaxation 3) Pancreatic enzyme and HCO3 secretion 4) Inc growth of exocrine pancreas and gallbladder 5) Inhibits gastric emptying
GIP: Source
K cells in duodenum
GIP: Stimulus
1) ORAL glucose 2) Fats 3) Amino acids
GIP: Action
1) Inc insulin secretion 2) Inhibits gastric emptying
Motilin: Source
M cells in duodenum and jejunum
Motilin: Stimulus
Fasting
Gastrin: Most potent stimuli
1) Phenylalanine 2) Tryptophan
GI hormones: Neurocrine from vagus to gastrin
GRP/bombesin
GI hormones: An incretin
1) GIP 2) GLP-1
GI hormones: Responsible for inter digestive myoelectric complex
Motilin
Pancreatic polypeptide: Secreted by pancreas in response to
CHO, CHON, and lipids
Pancreatic polypeptide: Inhibits
Pancreatic HCO3 and enzymes
Enteroglucagon: Stimulus
Hypoglycemia
GLP-1: Source
L cells
GLP-1: Action
Stimulates insulin secretion
Secreted by cells throughout GIT in response to H+
Somatostatin
Somatostatin: Action
Inhibits release of all GI hormones
Secreted by mast cells of gastric mucosa
Histamine
Histamine: Action
1) Inc H+ secretion 2) Potentiates gastrin action 3) Potentiates Ach action
GI neurotransmitters that cause smooth muscle contraction
1) Ach 2) Enkephalins/opiates 3) Substance P
Satiety center
Vuchog Ventromedial hypothalamus
Hunger center
Lamon Lateral hypothalamus
Sends signals to satiety/hunger centers
Arcuate nucleus
Release POMC
Anorexogenic neurons
Release Neuropeptide Y
Orexigenic neurons
Stimulates anorexigenic neurons and inhibits orexigenic neurons
Leptin
Inhibits anorexigenic neurons
Ghrelin
Inhibits Ghrelin
Peptide YY
GI contraction: Due to sub threshold slow waves
Tonic
Tonic contractions are seen in
GI sphincters
GI contraction: Due to spike potentials
Phasic
Slow waves vs spike potentials: True action potential
Spike potentials
Slow waves are generated by this intrinsic GI pacemaker
Interstitial cells of Cajal
Slow waves: Slowest frequency at
Stomach
Slow waves: Fastest frequency at
Small intestines
Slow waves: Depolarization due to __ influx
Na
Spike potentials: Depolarization due to __ influx
Ca
Spike potentials: Threshold
-40mV
Most common stimulus for GI peristalsis
Distention of gut
Reflex: Muscles upstream contract, muscles downstream exhibit receptive relaxation
Myenteric reflex
Cannon’s law of the gut
Peristalsis always proceeds in the oral-aboral direction
Effectual peristalsis requires
An active myenteric plexus
T/F: Chewing can be involuntary
T
Swallowing center
Medulla
Phases of swallowing
1) Oral phase 2) Pharyngeal phase 3) Esophageal phase
Phases of swallowing: Oral phase is triggered by presence of food at
Pharynx
Phases of swallowing: T/F Oral phase is voluntary
T
Phases of swallowing: Relaxation of UES
Pharyngeal phase
Phases of swallowing: Prevents aspiration
Pharyngeal phase
Phases of swallowing: Closes UES
Esophageal phase
Esophageal peristaltic contraction: Creates pressure behind bolus of food
Primary
Esophageal peristaltic contraction: Clears oesophagus of remaining food
Secondary
Esophageal peristaltic contraction: Accelerated by gravity
Primary
Esophageal peristaltic contraction: Relaxation of LES is mediated by
Vagus nerve using VIP
Stomach: 2 functional divisions
1) Orad stomach: Upper 2/3 2) Caudad: Lower 1/3 + antrum
Stomach: Capacity once fully relaxed
0.8-1.5L
Stomach, functional divisions: Thin-walled
Orad
Stomach, functional divisions: Thick-walled
Caudad
Receptive relaxation of orad stomach is mediated by
Vagus nerve using Ach
Increases distensibility of orad stomach
CCK
Caudad stomach: Frequency of contraction
3-5x per minute
Caudad stomach: Frequency of additional contractions
Every 90 minutes
Caudad stomach: Additional contractions mediated by
Motilin
Size required to enter duodenum
Less than 1 mm3
Inhibitors of gastric emptying
1) CCK 2) H+ in duodenum
Small intestinal motility: Back-and-forth movement with no net forward motion
Segmentation contraction
Small intestinal motility: Propels chyme towards large intestine
Peristaltic contraction
Large intestine: Saclike segments due to segmental contractions
Haustra
Proximal colon is for
Absorption
Distal colon is for
Storage
Mass movements in the LI: Frequency
1-3x a day
Mass movements in the LI: Segments
Transverse colon to sigmoid colon
T/F Circular and longitudinal muscles are reciprocally innervated such that when 1 is contracted, the other is relaxed
T
Segmental vs peristaltic contraction: Haustra
Segmental
Stimulus for internal anal sphincter relaxation
Rectal contents
Reflex whereby rectal contents cause internal anal sphincter relaxation
Rectosphincteric reflex
Urge to defecate is felt once rectum is ___ filled
25%
Combustible material from feces
Methane
Gastroileal reflex
Food in stomach increases peristalsis in the ileum and relaxation of ileocecal sphincter
Gastrocolic reflex
Food in the stomach increases peristalsis in the colon and frequency of mass movements
Gastrocolic reflex is mediated by (3)
1) PSY nervous system 2) CCK 3) Gastrin
Reverse peristalsis that results in vomiting begins from what segment of the GIT
Small intestines
Vomiting center
Medulla (area postrema)
Send inputs to the vomiting center
1) Chemoreceptor trigger zone 2) Vestibular system 3) Back of throat 4) GIT
Average daily amount: Saliva
1L
Average daily amount: Gastric secretion
1.5L
Average daily amount: Pancreatic secretion
1L
Average daily amount: Bile
1L
Average daily amount: SI secretion
1.8L
Average daily amount: Brunner gland secretion
200mL
Average daily amount: LI secretion
200mL
Average daily amount: Total GIT secretion
6.7L
pH: Saliva
6-7
pH: Gastric secretion
1-3.5
pH: Pancreatic secretion
8-8.3
pH: Bile
7.8
Submucosal duodenal glands
Brunner’s glands
Salivary enzyme: Initial digestion of starch
Ptyalin (α-amylase)
Salivary enzyme: Initial digestion of lipids
Lingual lipase
T/F Lingual lipase is secreted in the saliva in its activated form
F
Phases of salivary secretion
1) Cephalic 2) Buccal 3) Esophageal 4) Gastric
Steps in formation of saliva
1) Primary secretion 2) Modification
Formation of saliva: Cells responsible for primary secretion
Acinar
Formation of saliva: Cells responsible for modification
Ductal
Formation of saliva: Primary secretion vs modification, secretion of isotonic saliva
Primary secretion
Formation of saliva: Steps in modification
1) Reabsorption of Na and Cl 2) Secretion of K and HCO3
Principal glands of salivation
1) Parotid 2) Submandibular 3) Sublingual
Serous vs mucinous: Ptyalin
Serous
Serous vs mucinous: Parotid gland
Serous
Serous vs mucinous: Submandibular gland
Mixed
Serous vs mucinous: Sublingual gland
Mixed
Increases vs decreases salivation: PSY nervous system
Increases
Increases vs decreases salivation: SY nervous system
Decreases
PSY vs SY: Saliva high in electrolytes but low in proteins
PSY
PSY vs SY: Saliva viscid and rich
SY
Initial vs final saliva: High in Na and Cl
Initial
Initial vs final saliva: High in HCO3 and K
Final
Formation of saliva: Hormone involved in reabsorption of Na by the ductal cells
Aldosterone
High vs low flow rate (saliva): High in Na, Cl, HCO3; Low K
High
High vs low flow rate (saliva): Low in Na, Cl, HCO3; High K
Low
Serous vs mucinous: Buccal glands
Mucinous
Initial vs final saliva: Na and Cl content less than in plasma
Initial and final
Initial vs final saliva: K and HCO3 higher than in plasma
Final
Components of gastric secretion (3)
1) HCl and pepsinogen 2) IF 3) Mucus
GIT segment: Vitamin B12 absorption
Ileum
Cell type-location: Parietal cells
Body
Cell type-location: Chief cells
Body
Cell type-location: G cells
Antrum
Cell type-location: Mucous cells
Antrum
Cell-secretion: Parietal cells
1) HCl 2) IF
Cell-secretion: Chief cells
Pepsinogen
Cell-secretion: G cells
Gastrin
Cell-secretion: Mucous cells
Mucus
Gland-location: Oxyntic glands
Body
Gland-location: Pyloric glands
Antrum
Gland-cells: Oxyntic glands
1) Mucus neck cells 2) Parietal cells 3) Chief cells
Gland-cells: Pyloric glands
1) G cells 2) Mucus cells
Cell-secretion: Mucus cells and mucus neck cells
1) Mucus 2) HCO3
Cell-secretion: Enterochromaffin cells
Serotonin
Cell-secretion: Enterochromaffin-like cells
Histamine
Chief cells are aka
Zymogen cells
Main gastric glands
Oxyntic glands
Progenitor of epithelial cells and glands of the stomach
Mucus neck cells
Parietal cells vs chief cells: Acidophilic
Parietal cells
Parietal cells vs chief cells: Basophilic
Chief cells
Transport mechanism: Secretion of H into gastric lumen
H-K ATPase
3 substances that stimulate gastric HCl secretion
1) Histamine 2) Acetylcholine 3) Gastrin
Gastric HCl secretion, stimulus: Paracrine
Histamine
Gastric HCl secretion, stimulus: Neurocrine
Ach
Gastric HCl secretion, stimulus: GI hormone
Gastrin
Parietal cell receptor: Histamine
H2
Parietal cell receptor: Ach
M3
Parietal cell receptor: Gastrin
CCKB
Inhibitors of gastric HCl secretion (3)
1) Somatostatin 2) pH
Somatostatin analog
Octerotide
Inhibitors of gastric HCl secretion, drug classes
1) H2-blocker 2) Anti-muscarinic 3) PPI
Inhibitors of gastric HCl secretion: H2 blocker
Ranitidine
Inhibitors of gastric HCl secretion: Anti-muscarinic
Atropine
Inhibitors of gastric HCl secretion: PPI
Omeprazole
Phases of HCl secretion
1) Cephalic 2) Gastric 3) Intestinal
Phases of HCl secretion: Responsible for majority of acid secretion
Gastric phase (60%)
Phases of HCl secretion: Least contributor to acid secretion
Intestinal phase (10%)
Stimuli for acid secretion: Intestinal phase
1) Amino acids 2) Peptides
Substances that protect mucosa from HCl and pepsin (3)
1) Mucin 2) HCO3 3) PG
Protective factors against PUD (3)
1) Mucosal blood flow 2) PG 3) Growth factors
Pancreatic secretion: High vs low volume
High
Pancreatic secretion: High vs low HCO3
High
Pancreatic secretion: Hypertonic vs isotonic vs hypotonic
Isotonic
Pancreatic secretion: Higher vs lower Na and K content than plasma
Equal
Pancreatic secretion: High vs low Cl
Low
Pancreatic secretion: Contents (4)
1) Pancreatic amylase 2) Lipase 3) Protease 4) Tryspin inhibitor
Pancreatic secretion: Phases
1) Cephalic 2) Gastric 3) Intestinal
Pancreatic secretion: Stimuli (3)
1) Secretin 2) CCK 3) Ach (PSY)
Pancreatic secretion, stimulus: Acts on ductal cells
Secretin
Pancreatic secretion, stimulus: Acts on ductal and acinar cells
1) CCK 2) Ach
Pancreatic secretion, stimulus-receptor: CCK
CCKA
Pancreatic secretion, stimulus-receptor: Ach
Muscarinic
Pancreatic secretion, stimulus: Potentiates effect of secretin in increasing HCO3
1) CCK 2) Ach
Sources of digestive enzymes: Carbohydrates
1) Saliva 2) Pancreas 3) Intestinal mucosa
Sources of digestive enzymes: Proteins
1) Stomach 2) Pancreas 3) Intestinal mucosa
Sources of digestive enzymes: Lipids
1) Saliva 2) Pancreas
Digestive enzyme for carbohydrates: Saliva
Amylase
Digestive enzyme for carbohydrates: Pancreas
Amylase
Digestive enzyme for carbohydrates: Intestinal mucosa (5)
1) Sucrase 2) Maltase 3) Lactase 4) Trehalase 5) α-dextrinase
Digestive enzyme for proteins: Stomach
Pepsin
Digestive enzyme for proteins: Pancreas (4)
1) Trypsin 2) Chymotrypsin 3) Carboxypeptidase 4) Elastase
Digestive enzyme for proteins: Intestinal mucosa (3)
1) Amino-oligopeptidase 2) Dipeptidase 3) Enterokinase
Digestive enzyme for lipids: Saliva
Lingual lipase
Digestive enzyme for lipids: Pancreas
1) Lipase-colipase 2) Phospholipase A2 3) Cholesterol ester hydrolase
Most common component of bile
Water
Active component of bile
Bile salts
Component of bile responsible for fat emulsification, absorption, and removal from body
Bile salts
Components of bile (6)
1) Water 2) Bile salts 3) Bilirubin 4) Cholesterol 5) Phospholipids 6) Electrolytes
Amount of bile in gallbladder
30-60 mL
T/F Liver bile = gallbladder bile
F
Most abundant substance secreted in bile (solute)
Bile salts
Bile salts accounts for ___% of solutes in bile
50`
Precursor of bile salts
Cholesterol
Primary bile acids (2)
1) Cholic acid 2) Chenodeoxycholic acid
Secondary bile acids (2)
1) Deoxycholic acid 2) Lithocholic acid
Site of synthesis: Primary bile acids
Liver
Site of synthesis: Secondary bile acids
Intesines (bacteria)
Site of synthesis: Bile salts
Liver
Enzyme for synthesis: Primary bile acids
7α-hydroxylase
Enzyme for synthesis: Secondary bile acids
7α-dehydroxylase
Direct precursor: Primary bile acids
Cholesterol
Direct precursor: Secondary bile acids
Primary bile acids
Direct precursor: Bile salts
Secondary bile acids
Process by which secondary bile acids are converted into bile salts
Conjugation
Bile is concentrated in what organ
Gallbladder
Substances that cause GB contraction
1) CCK 2) Ach (PSY)
Most potent stimulus for sphincter of Oddi relaxation
CCK
T/F Bile is released in PULSATILE spurts
T
% bile salts recirculated back to the liver
94%
Where bile salts are reabsorbed for recirculation
Terminal ileum
Transporter responsible for reabsorption of bile salts in the terminal ileum
Na-bile contransporter
Substance that causes secretion of ions and water into bile before being reabsorbed in the gallbladder (concentration)
Secretin
Hyper- vs iso- vs hypotonic: Saliva
Hypotonic
Factors that increase secretion: Saliva
1) PSY (prominent) 2) SY
Factors that increase secretion: Pepsinogen and IF
PSY
Factors that decrease secretion: Saliva
1) Sleep 2) Dehydration 3) Atropine
Increase vs decrease gastric secretion: Chyme in duodenum
Decrease
Factors that decrease secretion: Bile
Ileal resection
GI surface area for absorption
250 m2
Only form of carbohydrates absorbed in the GIT
Monosaccharides
Starch is digested by ptyalin to form
1) α-dextrins 2) Maltose 3) Maltotriose
Enzyme that digests maltotriose to form glucose
Sucrase
Trehalose > trehalase =
Glucose
Lactose > lactase =
Glucose + galactose
Sucrose > sucrase =
Glucose + fructose
Transporter: Glucose and galactose from lumen to intestinal cell
SGLT-1
Transporter: Fructose from lumen to intestinal cell
GLUT-5
Transporter: Glucose, galactose, and fructose from intestinal cell to bloodstream
GLUT-2 (and GLUT-5)
Passive vs active: SGLT-1
Active (secondary active)
Passive vs active: GLUT-2
Passive uniport
Passive vs active: GLUT-5
Passive uniport
Form of protein absorbed from the GIT
1) Amino acids 2) Dipeptides 3) Tripeptides
Transporter: Tripeptides and dipeptides
H-dependent cotransport
Transporter: Amino acids
Na-aa cotransport
Activator of pepsinogen
Low pH
Activators of trypsinogen (2)
1) Trypsin (activates itself) 2) Enterokinase from intestinal brush border)
Enzymes activated by trypsin
1) Trypsinogen 2) Chymotrypsinogen 3) Proelastase 4) Procarboxypeptidase A 5) Procarboxypeptidase B
Optimum pH for pepsin activity
1-3
pH at which pepsin is inactivated
>5.0
Optimum pH at which lipase is activated
7.5-8
T/F Pepsin is essential for protein digestion
F
T/F Trypsin is essential for protein digestion
T
Site of lingual lipase activation
Stomach
Site of gastric lipase activation
Stomach
Site of pancreatic lipase activation
Small intestine
Form of fat absorbed from intestinal lumen to intestinal cell
Micelle
Form of fat absorbed from intestinal cell to lacteals
Chylomicrons
Enzyme for digestion: TAG
Lingual, gastric, and pancreatic lipase
Enzyme for digestion: Cholesterol ester
Cholesterol ester hydrolase
Enzyme for digestion: Phospholipid
Phospholipase A2
Triglyceride > lipase
Monoglyceride + 2 FA
Cholesterol ester + cholesterol ester hydrolase
Cholesterol + FA
Phospholipid + phospholipase A2
Lysolecithin + FA
Monoglyceride is made of
1 glycerol + 1 FA
Cholesterol ester is made of
Cholesterol + FFA
TG is made of
MG + FFA
Phospholipid is made of
Lysophospholipid + FFA
Chylomicron is absorbed from intestinal cell through what transport mechanism
Exocytosis
Mechanism by which micelles are absorbed from intestinal lumen to intestinal cell
Passive diffusion
Form of fat that does not need to be processed by SER in the intestinal cell form absorption into lacteals, instead are directly absorbed
Short- and medium-chain fatty acids
Inactivate pancreatic lipase
Bile salts
Coenzyme secreted by pancreas to prevent inactivation of pancreatic lipase by bile salts
Colipase from procolipase
Enzyme: Procolipase > lipase
Trypsin
Only product of TG metabolism that is not hydrophobic
???
Components of TAG
1) Glycerol 2) 3 FAs
GIT: Main site for water absorption
LI
GIT: Potassium absorption
SI
GIT: Potassium secretion
LI
GIT: Primary ion secreted in intestinal lumen
Cl-
GIT: Needed for absorption of Ca
1,25-dihydroxycholecalciferol
GIT: Needed for iron absorption
Vitamin C
GIT: Vitamins whose metabolism involves normal colonic flora
K, B1, B2, B12
Substances absorbed in ileum
1) Vitamin B12 2) Bile salts
GI transport mechanism of water-soluble vitamins
Na-dependent cotransport
GI transport mechanism: Calcium
Vitamin D-dependent Ca-binding protein
GI transport mechanism: Iron, intestinal cell
Apoferritin
GI transport mechanism: Iron, bloodstream
Transferrin
% body weight: Liver
2
% cardiac output: Liver
25
Phase I vs Phase 2 metabolism: CYP450 enzymes
Phase I
Bilirubin metabolism
Functional unit of liver
Lobule
Liver lobule: Shape
Hexagonal
Liver lobule: Center
Central vein (hepatic vein)
Liver lobule: Borders
Portal triad
Liver lobule, zone: Periportal
Zone 1
Liver lobule, zone: Midzonal
Zone 2
Liver lobule, zone: Centrilobular
Zone 3
Liver can regenerate up to ___% of lost mass
70
Condition for optimal liver regeneration
Must not be accompanied by viral infection or inflammation
Liver macrophage
Kupffer cells
T/F Kupffer cells are extremely effective in blood cleansing that less than 1% of bacteria make it to the systemic circulation
T
Special liver cells: Found in space of Disse
Ito cells
Special liver cells: Found in liver sinusoids
Kupffer cells
Special liver cells: Vitamin A storage
Ito cells
Special liver cells: APC
Kupffer cells
Water-soluble vitamins
B and C
Fat-soluble vitamins
ADEK
