Block 6 Exam Flashcards
Mouth
Mechanical homogenization of food
Salivary glands
Salivary secretion
Hydration, lubrication, Amylase
Esophagus
Propulsion of food
Stomach
Gastric acid & pepsinogen secretion, mechanical churning to reduce particle size
Pancreas
Pancreatic secretion of bicarbonate, propeptidases, amylase, prolipases
Liver and Gall bladder
Bile acid secretion
Small intestine
Digestion and absorption of nutrients (proteins, fats, sugars), electrolytes, and water
Anus
Defecation of fecal waste
Villi cells
Primarily nutrient and electrolyte absorption
Crypt or gland cells
Primarily secretion
Features that increase surface area of small and large intestine
Folds of Kerckring Semilunar folds Villi Crypts or glands Microvilli
Transcellular
Through the cell
Paracellular
Between the cell
Blood flow in fasting state
30mL/min/100g of tissue
Blood flow after a meal
Can reach 250mL/min/100g of tissue
Which locally produced hormones and kinins cause vasodilation during digestion
Cholecystokinin
Neurotensin
Submucosal plexus
Meisner’s
Only found in small and large intestine
Myenteric plexus
Auerbach’s
Found throughout GI tract
Vagovagal reflex
Sensory afferents from chemoreceptors, osmoreceptors, and mechanoreceptors in the mucosa are carried by the vagus nerve to autonomic centers in the brain, which in turn sends efferents via the vagus nerve to change secretion and motility
Acetylcholine (ACh) source
Cholinergic neurons
Acetylcholine (ACh) Actions
Contraction of smooth muscle in wall Relaxation of sphincters Increase salivary secretion Increase gastric secretion Increase pancreatic secretion
Norepinephrine (NE) source
Adrenergic neurons
Norepinephrine (NE) actions
Relaxation of smooth muscle in wall
Contraction of sphincters
Increase salivary secretion
Vasoactive intestinal peptide (VIP) source
Neurons of mucosa and smooth muscle
Vasoactive intestinal peptide (VIP) actions
Relaxation of smooth muscle
Increase intestinal secretion
Increase pancreatic secretion
Gastrin-Releasing Peptide (GRP), or Bombesin source
Neurons of gastric mucosa
Gastrin-Releasing Peptide (GRP), or Bombesin actions
Increase gastrin secretion
Enkephalins (opiates) source
Neurons of mucosa and smooth muscle
Enkephalins (opiates) actions
Contraction of smooth muscle
Decrease intestinal secretion
Neuropeptide Y source
Neurons of mucosa and smooth muscle
Neuropeptide Y actions
Relaxation of smooth muscle
Decrease intestinal secretion
Substance P source
Cosecreted with ACh
Substance P actions
Contraction of smooth muscle
Increase salivary secretion
Cholecystokinin source
I cells in duodenum and jejunum
Neurons in ileum and colon
Cholecystokinin target
Pancreas
Gall bladder
Cholecystokinin action
Increase enzyme secretion (pancreas) Increase contraction (gall bladder)
Gastric inhibitory peptide source
K cells in duodenum and jejunum
Gastric inhibitory peptide target
Pancreas
Gastric inhibitory peptide action
Exocrine: decrease fluid absorption
Endocrine: increase insulin release
Suppresses glucagon secretion
Gastrin source
G cells, antrum of stomach
Gastrin target
Parietal cells in body of stomach
Gastrin action
Increase H+ release
Gastrin-releasing peptide source
Vagal nerve endings
Gastrin-releasing peptide target
G cells in antrum of stomach
Gastrin-releasing peptide action
Increase gastrin release
Guanylin source
Ileum and colon
Guanylin target
Small and large intestine
Guanylin action
Increase fluid absorption
Motilin source
Endocrine cells in upper GI tract
Motilin target
Esophageal sphincter
Stomach
Duodenum
Motilin action
Increase smooth-muscle contraction
Migrating motor complex
Neurotensin source
Endocrine cells
Widespread in GI tract
Neurotensin target
Intestinal smooth muscle
Neurotensin action
Vasoactive stimulation of histamine release
Peptide YY source
Endocrine cells in ileum and colon
Peptide YY target
Stomach
Pancreas
Peptide YY action
Decrease vagally mediated acid secretion (stomach)
Decrease enzyme and fluid secretion (pancreas)
Secretin source
S cells in small intestine
Secretin target
Pancreas
Stomach
Secretin action
Increase HCO3 - and fluid secretion by pancreatic ducts (pancreas)
Decrease gastric acid secretion (stomach)
Somatostatin source
D cells of stomach and duodenum
Somatostatin target
Stomach
Intestine
Pancreas
Liver
Somatostatin action
Decrease gastrin release (stomach)
Increase fluid absorption/decrease secretion (intestine)
Increase smooth-muscle contraction (intestine)
Decrease endocrine/exocrine secretions (pancreas)
Decrease bile flow (liver)
Substance P source
Enteric neurons
Substance P target
Enteric neurons
Substance P action
Neurotransmitter
VIP source
ENS neurons
VIP target
Small intestine
Pancreas
VIP action
Increase smooth-muscle relaxation (small intestine)
Increase secretion by small intestine (small intestine)
Increase secretion by pancreas (pancreas)
Peristalsis
Propulsion of chyme in the caudal direction
Segmentation
Mixing or churning of chyme
Gastric accommodation
Active dilation or relaxation of the fundus of the stomach in response to entry of food
Internal anal sphincter
Circular and longitudinal smooth muscle
Involuntary control
External anal sphincter
Striated muscle only
Voluntary and involuntary control
What portions of the human digestive system contain striated muscle
Upper esophageal sphincter
Upper third of esophagus
External anal sphincter
Principal functions of stomach
Stores and mixes food
Secretes intrinsic factor for vitamin B12 absorption
Secretes HCl and proteolytic enzymes
Exocrine secretions of stomach
Facilitate iron absorption
Secretes mucus to protect mucosa against noxious agents
Endocrine secretions of stomach
Miscellaneous functions
Gastric Sympathetic innervation function
Decrease motility
Decrease secretion
Constrict vasculature
Where is pepsinogen I released from
Oxyntic mucosa only
Where is pepsinogen II released from
Throughout gastric mucosa
Gastric endocrine cells neurotransmitters
Vasoactive intestinal peptide (VIP) Galanin Serotonin Pituitary adenylate cyclase activating peptide (PACAP) Gastrin-releasing peptide (GRP)
Gastric endocrine cells paracrine mediators and hormones
Ghrelin
Gastrin
Somatostatin
Loss of sonic hedgehog
Loss of acidity
Diminished production of somatostatin
Increase in serum gastrin levels
What do parietal cells release
intrinsic factor
HCl
What do chief cells release
pepsinogen
What do ECL cells release
histamine
What do G cells release
gastrin
GF
What do D cells release
somatostatin
What cells does ACh act on
Parietal cell
ECL cell
D cell
ACh receptor
M3
What cells does GRP act on
G cell
Atropine
Blocks M3 receptor
Cimetidine, Ranitidine (-dine)
Block H2 receptor
Omeprazole, Pantoprazole (-azole)
PPI
ANTGIP effect on plasma insulin
Decreases
ANTGIP effect on serum glucose levels
Decrease
Gastrin’s role in duodenal ulcer
Basal levels slightly elevated
Meal-stimulated elevated, prolonged
Autoregulatory defect
Increased responsiveness of parietal cells to circulating gastrin
Somatostatin Inhibits which GI functions
GI peptides
Gastric acid secretion
Motility
Pancreatic enzyme and HCO3- secretion
Somatostatin mode of action
Neurotransmitter
Hormone
Paracrine
Duodenal ulcer phenotype
Antral predominant gastritis
High gastrin and acid secretion
Impaired inhibitory control of acid secretion
Protection from gastric cancer
Simple gastritis phenotype
Mild mixed gastritis
High gastrin but normal acid secretion
No gastric atrophy
No significant clinical outcome
Gastric cancer phenotype
Corpus-predominant gastritis Multi-focal atrophic gastritis High gastrin Hypo/achlorhydria Low pepsinogen I and pepsinogen I/II ratio Increased risk of gastric cancer
Invasive methods to diagnose H. pylori
Histology
Culture
Rapid urease test (CLOtest)
Serology to diagnose H. pylori
ELISAs detect IgG
Best test for evaluating eradication of H. pylori
Urea breath tests
Past treatment of peptic ulcer
No acid, no ulcer
Acid suppression
Present treatment of peptic ulcer
Cure H. pylori, heal ulcer
H. pylori eradication and acid suppression
Future treatment of peptic ulcer
No H. pylori, no ulcer
Prevent ulcer by preventing H. pylori
What are incretins
Hormones mediating the enteroinsular axis
Incretin stimulus
Glucose containing meal
Site of release of incretins
Small intestine
Effect of incretin release
Stimulated pancreatic beta islet cells to release insulin
Pathologies of Gastric Inhibitory Polypeptide
Obesity and type 2 Diabetes mellitus
Cushing’s syndrome
GIP synthestized/secreted by what?
K cells in upper small intestine
GIP biological properties
Delays gastric emptying
Stimulates insulin release in response to glucose
Effects of GIP on metabolism
Increase insulin release
Increase glucose absorption
Decrease lipolysis
Increase lipogenesis/fat storage
Effects of ANTGIP on metabolism
Decrease GIP stimulated insulin release
Decrease serum glucose levels
Decrease d-glucose absorption from the small intestine
Increase lipolysis
Metabolic syndrome characterized by
Obesity
Nonalcoholic fatty liver disease (NAFLD)
Insulin resistance with hyperinsulinemia
Duodenal ulcer
Damage to duodenal mucosa via excessive gastric acid secretion
Gastric ulcer
Damage to gastric mucosa via cytotoxic atrophy
H. pylori in Duodenal ulcer
Inhibits somatostatin and HCO3- secretion
Hypersecretory states in duodenal ulcer
Elevated basal gastrin
Significantly increased postprandial gastrin secretion
H. pylori in gastric ulcer
Release cytotoxins that damage gastric mucosa
Decrease in gastric [H+] in gastric ulcer
H. pylori migrates to corpus and damages/inhibits parietal cells and increases gastric secretion
Functions of saliva
Moisten and lubricate foodstuffs Facilitate speech Dissolve food for taste Begin digestion of carbohydrates and lipids Antibacterial/immunologic Retards dental caries Washes out substances
Types of acinar cells
Serous
Mucus
Serous acinar cell
water
salts
protin
Mucus acinar cell
Mucins
Exocrine pancreas function
Secretion of bicarbonate to neutralize gastric acid
Secretion of digestive enzymes
Ductal cell bicarbonate secretion inhibited by
substance p
Ductal cell bicarbonate secretion stimulated by
ACh
Secretin
Parotid acinar cell
alpha-amylase
Sublingual acinar cell
Mucin glycoprotein
Aldosterone effect on salivary ductal cells
Increase absorption of NaCl and secretion of K+
Increase ENaC
Most important regulator of Protein secretion by pancreatic acinar cells
ACh
Most potent regulator of Protein secretion by pancreatic acinar cells
CCK
Most potent 2nd messenger of Protein secretion by pancreatic acinar cells
Ca2+
Ductal cell Cl- secretion facilitated by
Apical CFTR and CaCC
Basolateral channels on ductal cells
Sodium bicarb co-transporter
Bicarb from CO2 and carbonic anhydrase
Apical channels on ductal cells
Leaves by anion exchanger
Pancreatic secretion cephalic phase regulated by
ACh
Pancreatic secretion intestinal phase regulated by
CCK
Secretin
Vagovagal enteropancreatic reflex
What does CCK cause exocrine pancreas
Maximal acinar release of digestive enzyme
What does secretin cause exocrine pancreas
Maximal ductal secretion of HCO3- and fluid
CCK effect on bile release
Contraction of gallbladder
Relaxes sphincter of Oddi
ACh effect on bile release
Contraction of gall bladder
Principle roles of bile
Gastric acid neutralization
Assist with lipid absorption
Nutrients that trigger GIP release
Proteins
Lipids
Carbohydrates
Nutrients that trigger Secretin release
H+
Fatty acids
Nutrients that trigger Gastrin release
Amino acids/peptones
Vagal stimulation
Nutrients that trigger CCK release
Fatty acids»_space; proteins
Na/glucose or Na/Amino acid cotransporters timing
Primary mechanism after a meal
Na/glucose or Na/amino acid cotransporters location
Duodenum
Jejunum (main)
Ileum
Na-H exchanger timing
Postprandial
Na-H exchanger location
Duodenum Jejunum (main)
Parallel Na-H and Cl-HCO3 exchanger timing
primary mechanism during interdigestive period
Parallel Na-H and Cl-HCO3 exchanger location
Ileum
Proximal colon
Epithelial Na+ channel (ENaC) location
Distal colon
Passive K+ absorption location
Jejunum
Ileum
Passive K+ secretion location
Proximal colon Distal colon (main)
Active K+ secretion location
Proximal colon (main) Distal colon
Active K+ absorption location
Distal colon
Na/Glucose or Na/Amino acid cotransporters enterotoxin effect
No effect
Parallel Na-H and Cl-HCO3 exchanger enterotoxin effect
Decreases Na+ absorption
What inhibits ENaC
Amiloride
What enhances ENaC
Aldosterone
Active K+ secretion stimulation
cAMP, Ca2+
Active K+ secretion enhanced by
Aldosterone
Small intestine K+ transport
Net absorption
Large intestine K+ transport
Net secretion
Passive Cl- absorption timing
During a meal
Passive Cl- absorption location
Jejunum (main)
Ileum (limited)
Distal colon (main)
Cl-HCO3 exchanger timing
Interdigestive
Cl-HCO3 exchanger location
Ileum
Proximal colon (main)
Distal colon
Cl- Secretion location
Duodenum Jejunum Ileum Proximal colon Distal colon
Bacterial enterotoxins secretagogue
Cholera toxin
E. coli; heat labile and heat stable
Yersinia toxin
Clostridium difficile toxin
Cholera toxin second messenger
cAMP
E. coli heat labile second messenger
cAMP
E. coli heat stable second messenger
cGMP
Yersinia toxin second messenger
cGMP
Clostridium difficile toxin second messenger
Ca2+
Hormones and neurotransmitters secretagogue
VIP Guanylin Acetylcholine Bradykinin Serotonin (5-HT)
VIP second messenger
cAMP
Guanylin second messenger
cGMP
Acetylcholine second messenger
Ca2+
Bradykinin second messenger
Ca2+
Serotonin (5-HT) second messenger
Ca2+
Immune cell products secretagogue
Histamine
Prostaglandins
Histamine second messenger
cAMP
Prostaglandins second messenger
cAMP
Laxatives secretagogue
Bile acids
Ricinoleic acid
Bile acid second messenger
Ca2+
Lamina Propria cells affect on intestinal ion transport Macrophages
Prostaglandins
O2 radicals
Lamina Propria cells affect on intestinal ion transport Mast cells
Histamine
Lamina Propria cells affect on intestinal ion transport neutrophils
Eicosanoids
Platelet-activating factor
Lamina Propria cells affect on intestinal ion transport fibroblasts
Eicosanoids
Bradykinin
Sucrose
Glucose + fructose
Lactose
Glucose + Galactose
Maltose
2 glucose
Maltotriose
3 glucose
Lactase deficiency causes
Physiological
Familial
Decreased mucosal surface area
Damage to enterocytes
Lactase deficiency problems
Milk intolerance
Flatulence/distention
Diarrhea
Cramps
Trypsinogen activating agent
Enteropeptidase
Trypsin
Trypsinogen active enzyme
Trypsin
Trypsinogen action
endopeptidase
Trypsinogen products
Oligopeptides (2-6 amino acids)
Chymotrypsinogen activating agent
Trypsin
Chymotrypsinogen active enzyme
Chymotrypsin
Chymotrypsinogen action
Endopeptidase
Chymotrypsinogen products
Oligopeptides (2-6 amino acids)
Proelastase activating agent
Trypsin
Proelastase active enzyme
Elastase
Proelastase action
Endopeptidase
Proelastase products
Oligopeptides (2-6 amino acids)
Procarboxypeptidase A activating agent
Trypsin
Procarboxypeptidase A active enzyme
Carboxypeptidase A
Procarboxypeptidase A Action
Exopeptidase
Procarboxypeptidase A products
Single amino acids
Procarboxypeptidase B activating agent
Trypsin
Procarboxypeptidase B active enzyme
Carboxypeptidase B
Procarboxypeptidase B action
Exopeptidase
Procarboxypeptidase B products
Single amino acids
Peyer’s patches
Aggregated lymphoid tissue in lamina propria
Detergents
Amphipathic molecules that are water-soluble below CMC and form micelles above CMC
Emulsifiers
Amphipathic molecules that can be incorporated into micelles
Surfactants
Amphipathic molecules that helps stabilize two non-mixable fluids
Why do we need cholesterol
Makes membranes pliable, yet tight
Where does cholesterol come from
Synthesized by liver
Diet
How do we get rid of cholesterol
Predominantly by bile acid synthesis
Bad properties of cholesterol
Insoluble in water
Limited lipid solubility
Forms crystals when lipids are saturated
Gut derived lipoproteins
Chylomicrons
Remnant chylomicrons
Liver derived lipoproteins
VLDL
LDL
HDL
Chylomicrons core
TAGs
Vitamins A, E, and K
Cholesterol
Cholesterol esters
Chylomicrons surface
Apolipoprotein A1
Phospholipids
Cholesterol
Cl- secretion stimulators
cAMP
cGMP
Ca2+
Carbohydrate absorption
Duodenum (main)
Jejunum
Ileum
Alpha-amylase produces:
Maltose
Maltotriose
alpha-limit dextrins
SGLT1 functions
Mediates glucose and galactose into enterocytes
GLUT5 function
Facilitated diffusion of fructose into enterocytes
GLUT2 function
Facilitated diffusion of all three monosaccharides out of the enterocytes
Isomaltase function
Breaks alpha 1,6 linkages
Oligopeptide abosrption
H/oligopeptide cotransporter
Amino acid absorption
Na/AA cotransporter
Where is cobalamin absorbed
Ileum
What stimulates intrinsic factor release
Histamine
ACh
Gastrin
Ca2+ absorption
Passive throughout small intestine
Active in duodenum
How does Ca2+ enter enterocyte
TRPV6 channel
How does Ca2+ exit enterocyte
Ca-H pump
Na-Ca exchanger
What is required for active Ca2+ absorption
Vitamin D
Calbindin
Keeps [Ca2+]i low
Driving force for more absorption
Ca2+ crucial second messenger to many pathways
Absorption of Folate location
Duodenum
Which form of iron is absorbed
Ferrous (Fe2+)
How does Fe2+ exit enterocyte
Ferroportin
Water soluble vitamins
B and C
Fat soluble vitamins
A
D
E
K
Anabolic functions in fed state
Glycogen synthesis
Lipogenesis
Protein synthesis
Catabolic functions in fasting state
Glycogenolysis
Lipolysis + Ketogenesis
Proteolysis
What ketone bodies do our bodies produce
Acetone
Acetoacetate
3-beta hydroxybutyrate
Glucose Homeostasis phase I
Brain uses glucose
Excess stored as glycogen
Cutoff @ 4 hours
Glucose Homeostasis Phase II
Short-term fasting between meals
Glycogen is used for glucose synthesis
Cutoff @ 16 hours
Glucose Homeostasis Phase III
Glycogen is depleted
Gluconeogenesis increases
Cutoff @ 2 days
Glucose Homeostasis Phase IV, V
Fuel sparing
Gluconeogenesis dips
Body relies on fats (keto acids)
What important gluconeogenic enzyme is the muscle missing
Glucose-6-Phosphatase
Phosphoglycerate kinase
1,3-BPG => 3-phosphoglycerate
Pyruvate kinase
PEP => Pyruvate
Glucokinase and Hexokinase
Glucose => Glucose-6-P
Phosphofructo-kinase-1
Fructose-6-P => Fructose-1,6-BP
Pyruvate dehydrogenase
Pyruvate => Acetyl CoA
Pyruvate carboxylase
Pyruvate => OAA
PEP carboxykinase
OAA => Phosphoenolpyruvate
Fructose bisphosphatase
Fructose-1,6-P => Fructose-6-P
Glucose 6-Phosphatase
Glucose-6-P => Glucose
Rate limiting step of glycolysis
PFK-1
Glucokinase glucokinase affinity
Low
Not easily saturated
Hexokinase glucose affinity
High
Saturable
Which enzyme is inhibited by G6P
Hexokinase
What upregulated PFK-1
F-2,6-BP
Malate-aspartate shuttle location
Liver and heart
What does the malate-aspartate shuttle produce
NADH
alpha-Glycerol phosphate shuttle location
Brain and muscle
What does the alpha-glycerol phosphate shuttle produce
FADH2