Exam 1 Physiology Flashcards
Form Soluble Complexes with Free Iron
1) Ascorbic Acid (Vitamin C)
2) Citric Acid
Myenteric Plexus
Network of enteric nervous system found throughout GI tract. Controls motility.
Inhibition of Gastrin Secretion
1) Somatostatin
2) Secretin
3) low pH
Monoglyceride Acylation Pathway
Triglyceride synthesized inside Enterocytes by:
1) 2-monoglyceride
2) CoA-activated Fatty Acids
Fatty-acid binding proteins then transport long-chain fatty acids to smooth ER for re-esterification
Primary Bile Acid
Synthesized directly in liver from cholesterol.
What does GRP stand for?
Gastrin-Releasing Peptide
Gastrocolic Reflex
Urge to defecate shortly after starting meal. Triggered by the presence of food in the stomach.
Causes increased colonic motility.
Peptides Regulating CCK Release
1) CCK-Releasing Peptide (CCK-RP)
2) Monitor Peptide
Cause of retrograde movement from Rectum to Sigmoid Colon
Frequency of Segmental Contractions greater in Rectum than Sigmoid Colon
Cause: Secretory Diarrhea
Caused by bacterial infection in intestine (V. Cholerae or E. coli) or a tumor. Enterotoxins from E. coli activate gunaylin receptors in intestine.
Treatment for Hirschsprung’s Disease
Removal of the aganglionic segment
Function of Intrinsic Factor
Bind Vitamin B12 to prevent acid degradation and allow for absorption in the Ileum
Insoluble Form of Mucus
Secreted by Surface Mucus Cells as gel forming unstirred layer over mucosa. HCO3 gets trapped in this layer, keeping surface pH near neutral.
Site of Carbohydrate Digestion
Brush Border Membrane (Small Intestine)
Mechanism for Di/Tripeptide Uptake into Enterocytes
- Faster than single amino acids.
- H-Dependent Co-Transporter Peptide Transporter 1 (PEPT1).
- Pairs with NHE (H/Na Exchanger) on same membrane
- Peptides then hydrolyzed into amino acids by Cytoplasmic Peptidases
Trigger of Somatostatin Release
Acid in the lumen
Transport Protein for Uptake of Short-Chain Fatty Acids
SCFA/Na Cotransporter (SMCT1)
Lipid Malabsorption: Conditions Affecting/Decreasing Absorbing Cells
1) Tropical Sprue (flattening of villi from inflammation)
2) Gluten Enteropathy / Celiac Sprue
Usually conjugated with Bile Salts
Glycine or Taurine
Basolateral Membrane Transporter Bringing Chlorine into Crypt Cell
NKCC1 Cotransporter (2Cl-K-Na)
Short-Chain Fatty Acids Generated by Colonic Flora
1) Acetate
2) Propionate
3) Butyrate
Location of Enkephalin Secretion
Nerves in Mucosa and Smooth Muscle of GI tract
Location of Guanylin Secretion
Intestines
Function of Histamine
Increases Gastric Acid Secretion
1) Directly – Acting on Parietal Cells
2) Indirectly – Potentiating Gastrin and ACh
Dominant Na Absorption Mechanisms: Duodenum and Jejunum
1) Na-Glucose or Na-AminoA Co-Transport
2) Na-H Exchange
Secretion of GLP-1
Triggered by ingested nutrients (proteins and carbs). Biphasic release: early release (minutes), later release (about an hour)
Secretion of PYY
Secreted by L cells in Intestine, in proportion to caloric load.
What form of mucus is not present in the resting stomach?
Soluble Form
Enzyme Converting Trypsinogen to Trypsin
Enterokinase. secreted by brush border in small intestine
Result of Excess Iron: Pancreas
Diabetes
Transporter for Bile Acids: Enterocyte -> Portal Blood
Organic Solute Transporter (OST)
Location of Histamine Release
Enterochromaffin-like (ECL) Cells in Stomach
Triggers of CCK Secretion
(In small intestine)
1) Small peptides / amino acids
2) fatty acids
3) Monoglycerides
Cause of Gastric Ulcers
Breakdown of protective barrier of stomach by acid/pepsin.
Location of Cholecystokinin (CCK) Secretion
I Cells of Proximal Small Intestine
Suppositories
Dosage inserted into (in this case) rectum for local and systemic action
Action of Ghrelin
Stimulates NPY and AgRP neurons.
Most Easily Absorbed Form of Iron
Heme Iron
Fructose absorption mechanic
Can only be by facilitated diffusion
Location of Intrinsic Factor Release
Parietal Cells of Gastric Mucosa
Starches digested by Salivary/Pancreatic α-amylases
1) Amylopectin
2) Amylose
Receptive Relaxation
Vagaovagal reflex where proximal stomach relaxes to accommodate an ingested meal
Function of Guanylin
Binds to Guanylyl Cyclase to increase Cl- secretion and thus fluid secretion
Na Absorption Mechanisms in Enterocytes
1) Restricted Diffusion
2) Na-Glucose or Na-AminoA Co-Transport
3) Na-Cl Co-Transport
4) Na-H Exchange
Cells generating Slow Waves
Interstitial Cells of Cajal
Location of GRP Release
Nerves in Gastric Mucosa
Breakdown Products of Pancreatic Enzyme Hydrolysis of Lipids
1) Fatty Acids
2) Monoglycerides
3) Lysophospholipids
4) Cholesterol
Functions of Leptin
1) Increase metabolic and energy expenditure rate (Sympathetics)
2) Decrease energy storing (by decreasing insulin secretion)
Leptin Actions on Arcuate Nucleus
Represses:
1) NPY
2) AgRP
Stimulates:
1) α-MSH
2) CART
Mucous Neck Cells (Oxyntic Gland)
Secrete mucus and serve as Stem Cells.
Activate CFTR Channels
Increase in cAMP or Ca2+ levels
Goblet Cells
Interspersed with enterocytes in small intestine. Secrete mucus
Bile-Dependent Biliary Secretion
Bile salts/acids stimulate bile SECRETION and inhibit bile SYNTHESIS.
Nucleus Tractus Solitarus (Brainstem)
Reciprocal connections between hypothalamus and NTS. Has a high density of Y Receptors (Y1 and Y5). Satiety center is also present.
Responds to:
1) Peripheral circulating signals
2) Vagal afferents from GI Tract (inhibitory)
Intestinal Phase of Pancreatic Secretion
1) S Cells release Secretin in Duodenum. Triggered by Acid/Fat/Protein in Duodenum. Secretin increases Ductule Cell HCO3 secretion.
2) I Cells release CCK in Duodenum. Triggered by Fat/Protein/CRP/Monitor Peptide. CCK acts on Acinar Cells to increase enzyme secretion
3) Vagovagal Reflexes triggered by acid/fat/protein
Hypothalamic Nuclei in Appetite/Energy Expenditure Regulation
1) Lateral Nuclei
2) Ventromedial Nucleus
3) Paraventricular Nucleus (PVN)
4) Dorsomedial Nucleus (DVN)
5) Arcuate Nucleus (ARC)
Pancreatic Enzymes Catalyzed by Trypsin
1) Autocatalysis
2) Chymotrypsinogen -> Chymotrypsin
3) Proelastase -> Elastase
Functions of VIP
1) Relaxation of smooth muscle (main)
2) Stimulates Intestinal/Pancreatic Secretion
Haustra
Sac-like segments in the colon, present when empty. Appear during contraction of a segment and then disappear after.
Inhibitors of Motilin Release
Eating
Pancreatic Lipase
Cleaves fatty acids from 1 and 3 positions of Triglycerides.
Produces:
1) two fatty acids
2) 2-monoglyceride
Brush Border Iron Importer
Ferrous Iron Transporter (DMT1)
Enzymes hydrolyzing oligosaccharides to glucose
1) Glucoseamylase
2) Isomaltase
3) Maltase
Cholelithiasis
Gallstones
Phospholipase A2
Releases fatty acids from 2 position of Phospholipids
Produces:
1) Lysophospholipids
2) Free Fatty Acids
Enzyme Types Which Digest Proteins
1) Endopeptidases
2) Exopeptidases
3) Peptidases in Brush Border
Cephalic and Gastric Phases of Pancreatic Secretion
MOSTLY DIGESTIVE ENZYMES
1) Distended Stomach -> ACh (Vagovagal) -> Acinar and Ductule Cells
2) CCK-RP and Monitor Peptide (nerve input) released
Peristaltic Reflex
Contraction moving contents along in small intestine. Initiated by chyme in the intestine (distention or irritation).
Mediated by Enteric Nervous System
Functions of Gastrin Secretion
1) Stimulate HCl secretion by Parietal Cells
2) Stimulate growth of gastric mucosa and motility
Phases of Acid Secretion
1) Basal Secretion
2) Cephalic Phase
3) Gastric Phase
4) Intestinal Phase
Bind to Bile Acids inside Ileal Enterocyte
Ileal Bile Acid Binding Protein (IBABP)
Mechanism for Amino Acid Uptake into Enterocytes
Na+-Dependent Co-Transport. Separate ones for neutral, acidic, basic, and imino amino acids. Moves into blood via facilitates diffusion
Location of Motilin Secretion
M Cells in Stomach and Small Intestine
Enterocytes
Most common cell in small intestine.
Function:
1) Digestion
2) Absorption
3) Secretion
Pathways for Heme Iron Uptake into Enterocytes
1) Receptor-Mediated Endocytosis
2) Transporter Protein HCP1
Cystinuria
Defect in uptake of basic amino acids in gut and kidney.
Basal Secretion (Acid Secretion)
In absence of stimulation. Associated with Circadian Rhythm.
Main Components of Flatus
1) N2 (Swallowed Air)
2) H2 and CO2 (Bacterial fermentation of sugars; CO2 also from acid reactions in stomach)
3) Methane in 1/3 of adults (genetic)
Orexin (Hypocretin)
Released by Hypothalamus during deprivation. Promotes food intake
Symptoms: Acute Pancreatitis
Severe abdominal pain, swollen/tender abdomen, nausea, vomiting, diarrhea, fever
Achalasia
Neuromuscular disorder of lower 2/3 esophagus, which has an absence of peristalsis and LES which fails to relax.
Causes food to accumulate in esophagus.
Gastric Lipase
Hydrolyzes Triglycerides into Diglycerides and Free Fatty Acids in the Stomach
Osmotic Diarrhea
Accumulation of nonreabsorbable solutes in small intestine
Exopeptidases
Hydrolyze one amino acid at a time from the C Terminus. Secreted from pancreas as proenzymes and activated by Trypsin.
Examples: Carboxypeptidases A and B
Function of Motilin
Stimulate Migrating Myoelectric Complexes in the Stomach and Intestine
Production of Ghrelin
1) Increases with weight loss
2) Increases with stress and sleep deprivation
3) Decreases with weight gain and exercise
4) (increase following gastric bypass surgery)
Proopiomelaocortin (POMC) Neurons
Decrease food intake and increase energy expenditure. Release α-MSH and CART. Have Nicotinic ACh Receptors which enhance firing.
Fold of Kerckring
Longitudinal folds in the Small Intestine to increase surface area
Ileus
Loss/reduction of contractile activity in small intestines in absence of obstruction as a result of the irritation of the peritoneum.
Caused by:
1) Surgery
2) Acute/Systemic Illness
3) Electrolyte Imbalance
4) Tricyclic Antidepressants
Gastric Phase (Acid Secretion)
Initiated by entry of food into stomach (both pH and distention). Stopped by negative feedback of acid in stomach.
(more detail in notes)
Bilirubin
Principal pigment in bile. Metabolite of hemoglobin. Heme breakdown product, first forming biliverdin then becoming bilirubin. Insoluble in water.
More readily absorbed form of Free Iron
Ferrous (Fe2+)
Gallbladder Modification of Liver Bile
Active Removal:
1) Na
2) Cl
3) HCO3
Osmotic Gradient Removal:
1) Water
Intestinal Phase (Acid Secretion)
Initiated by protein digestion products in the Duodenum. Proximal duodenum secretes gastrin.
Acid Secretion Mechanism: Acetylcholine
1) Binds Muscarinic Receptor on Parietal Cell
2) Activates Phospholipase C
3) Forms IP3
4) Ca2+ released as Second Messenger
CCK-Releasing Peptide (CCK-RP)
Peptide regulator of CCK release secreted by Paracrine Cells within Small Intestine epithelium
Transports Iron from Enterocyte to Plasma
Ferroportin
Production of Leptin
Adipocytes
1) Increased when amount of adipose tissue increases
2) Increased by Insulin
3) Inhibited by fasting and weight loss
H+ Levels in Duodenal Ulcers
Increased
Pathologies where VIP plays central role
1) Pancreatic Islet Cell Tumor
2) Pancreatic Cholera / Watery Diarrhea Syndrome
When do Migrating Myoelectric Complexes begin?
After two hours of fasting
Location of Serotonin Release
Enteric Neurons and ECL Cells
Triggers of GIP Release
(in small intestine)
1) Fatty acids
2) Glucose
3) Amino Acids (lesser extent)
Lesion of Dorsomedial Nucleus
Depresses eating beahvior
Precursor to GLP-1
Proglucagon
Acid Secretion Mechanism: Histamine
1) Binds to H2 Receptor on Parietal Cell
2) Activates Adenylate Cyclase
3) cAMP second messenger
Dominant Na Absorption Mechanism: Colon
Restricted Diffusion
Core Contents of Chylomicrons
1) Triglycerides
2) Esterified Cholesterol
3) Fat-Soluble Vitamins
Stimulants of Gastric Acid Secretion
1) Acetylcholine
2) Histamine
3) Gastrin
Location of GI Sympathetics Synapse
Prevertebral Ganglia
Glucagon-like Peptide-1 (GLP-1)
Anorexigenic peptide produced by L Cells (Ileum and Colon).
Dominant Na Absorption Mechanisms: Ileum
1) Na-Glucose or Na-AminoA Co-Transport
2) Na-Cl Co-Transport
3) Na-H Exchange
Agouti-Related Peptide (AgRP)
Orixgenic released from ARC Neurons. Natural antagonist of MCR-3 and MCR-4. Excessive formation due to mutation associated with obesity.
Release inhibited by Insulin.
Muscle forming Upper Esophageal Sphincter
Cricopharyngeal Muscle
Most Common Causes of Jaundice
1) Hemolytic Anemia
2) Obstruction of Bile Duct
3) Liver cell damage
Gastroparesis
Impaired or delayed gastric emptying. Most common cause is diabetes (neurodamage from glycosylated Vagal nerve proteins)
Functions of CCK
1) Stimulate Gall Bladder Contraction
2) Stimulate Pancreatic Enzyme Secretion
3) Potentiate Pancreatic Bicarbonate Secretion (Stimulated by Secretin)
4) Inhibits gastric emptying
Enzymes Cleaving Sucrose into Glucose and Fructose
Sucrase
Ca2+ and cAMP actions in Parietal Cell
[Apical Membrane]
1) Increase Concentration of H/K-ATPases
2) Increased Concentration of Cl Channels
Muscle forming Lower Esophageal Sphincter
No distinct muscle (just thickening)
Destination for Chylomicrons after leaving Enterocyte
Enter Lacteals, central lymphatic vessels in the Villi, through gaps in lymphatic endothelial cells. Too large to enter capillaries so they enter bloodstream in the Thoracic Duct
Rectospincteric Reflex
Relaxation of Internal Anal Sphincter after the Rectum contracts upon fecal matter being forced in. Involuntary
Lipid Malabsorption: Absence of Bile Salts
1) Liver Disease (ex: Hepatitis)
2) Obstruction of Common Bile Ducts by Gallstones
3) Bacterial Overgrowth of Small Intestines (deconjugate)
4) Increased Duodenal Acidity (bile salts less soluble)
Cholesterol Ester Hydrolase
Cleaves fatty acid from cholesterol esters.
Produces:
1) Free cholesterol
2) Fatty Acid
Protein Plug
High protein in Pancreatic Juice creates plug in ducts. Can lead to liver damage, malabsorption, steatorrhea
Mechanism of Action of GLP-1
1) Delays gastric emptying
2) Activates α-MSH and CART neurons
3) Inhibits AgRP and NPY Neurons
Ventromedial Nucleus
Satiety center. Has MC3R Melanocortin Receptor
Tehalose
Glucose Dimer
Mechanism of Pancreatitis
Activated enzymes digest pancreatic tissue. Enzymes leak into blood, increases serum amylase/lipase levels.
Surface Contents of Chylomicrons
1) Phospholipids
2) Apoprotein
3) Free Cholesterol
Physiological Functions of Colonic Flora
1) Digest Carbohydrates
2) Form Secondary Bile Acids and Deconjugate Bile Acids
3) Generate Short-Chain Fatty Acids `(absorbed by colon)
Soluble Form of Mucus
Secreted by Mucous Neck Cells after Vagal Stimulation. Mix with other secretions and lubricates chyme.
Actions of CCK on Gallbladder
1) Major Stimulator of Contraction (direct action on smooth muscle and indirectly via Vagus and Intrinsic Nerves)
2) Relaxes Sphincter of Oddi
Route for Na to follow Cl into intestinal lumen
Paracellular
Mechanism: Secretory Diarrhea
1) Activation of Cl channels (V. cholerae toxin causes constitutive activation)
2) Na and Water follow
3) Na reabsorption by Ileal Enterocytes via Cl Cotransport inhibited
Causes of Pancreatitis
Most Common: Alcoholism or Gallstones
Also: High triglycerides and smoking
Inhibited by Somatostatin
1) Gastric Acid Secretion
2) Gastrin Release
3) Release of all GI hormones
Enterocyte processing of Lysophospholipids
Combined with fatty acids to form phospholipid
Cholecystectomy
Removal of the gallbladder
Barret’s Esophagus
Metaplasia from long-term exposure to acid
Inflammatory / Infectious Diarrhea
Caused by infection by bacteria (salmonella, Campylobacter Clostridium difficile) or viruses (rotaviruses, norovirus)
Inflammatory and/or immune response kills intestinal cells.
Types of Gallstones
1) Cholesterol Type (most common)
2) Pigment Type
Hemochromatosis
Chronic over-absorption of Iron. Hereditary form is a defect in the HFE gene, causing Hepcidin levels to drop.
Cholestasis
Reduced or lack of bile flow. Can be caused by a defect in Hepatocyte BSEP pump.
Cocaine-Amphetamine-Regulated Transcript (CART)
Released from POMC Neurons. Also binds to MCR Receptors. Mutations can cause obesity.
Phases of Pancreatic Secretion
1) Basal (Insignificant)
2) Cephalic
3) Gastric
4) Intestinal (majority)
Bile-Independent Biliary Secretion
Volume of water and electrolytes secreted. Secretin stimulates secretion of HCO3 and water.
Gastroileal Reflex
Increased peristalsis in Ileum. Relaxation of Ileocecal sphincter so Ileal contents move into Large Intestine.
Triggered by gastric secretion and emptying
Surface Mucus Cells (Oxyntic Gland)
Extend into the duct’s opening
Triggers of Motilin Secretion
Just a cyclical release every 90 minutes
Neuropeptide Y (NPY)
Orixgenic which binds to Y Receptors (for example in Nucleus Tractus Solitarus).
Released when energy stores are low from ARC Neurons.
Inhibited by Enkephalin Release
Intestinal secretion of fluid and electrolytes
Cell Types in Oxyntic Gland
1) Mucous Neck Cells
2) Surface Mucus Cells
3) Parietal Cells
4) Chief Cells
5) Endocrine Cells
Crypt Cells
Stem cells in the Small Intestine (crypt base). Form both Enterocytes and Goblet Cells.
Secrete fluids and electrolytes.
Endopeptidases
Hydrolyze interior peptide bonds.
1) Gastric Pepsin
Pancreatic Enzymes
1) Trypsin
2) Chymotrypsin
3) Elastase
Ferritin
Cytosolic iron storage protein. Product of Iron + Apoferritin
Function of PYY
Anorexigenic. Reduces gastric emptying and delays intestinal transit.
Increased levels in disease state. Fasting plasma concentrations reduced in obesity.
What does GIP stand for?
Glucose-Dependent Insulinotropic Peptide
Appetite/Energy Expenditure Regulating Neurons in ARC
1) Propiomelocortin (POMC) Neurons
2) Orexigenic-Producing Neurons
Inhibitors of Gastric Emptying
1) Low pH
2) Presence of fat/protein digestion products
3) Non-Isotonic Solutions
4) Proximal Stomach Distention
5) Pressure in proximal Small Intestine
Function of Enkephalins
Stimulate contraction of Smooth Muscle
Especially Lower Esophageal, Pyloric and Ileocecal Sphincters
What does VIP stand for?
Vasoactive Intestinal Peptide
H+ Levels in Gastric Ulcers
Reduced (acid leaks into gastric mucosa and is lost)
Lipid Malabsorption: Failure to Digest Fat
Pancreatic enzymes either not secreted or inactivated by low pH
Ex: Pancreatitis, Pancreatic Carcinoma, Cystic Fibrosis
Salivary Glands (Ordered by amount)
1) Submaxillary
2) Parotid
3) Sublingual
Function of Centroacinar and Duct Cells
Secrete pancreatic juices with high bicarbonate concentration. Brings pH to optimal enzymatic range
Ductule/Centroacinar Cell Modification of Pancreatic Secretion
1) Secrete HCO3
2) Na follows HCO3
3) Absorb Cl
Trigger for GRP Release
Vagal Stimulation
Late Phase of Dumping Syndrome
Hypoglycemia 1-3 hours later. Rise in insulin means you absorb glucose too quickly.
Sweating, weakness, dizziness
Exception where both Parasympathetics and Sympathetics are Stimulatory
Both stimulate saliva secretion with ACh!
Oxyntic Gland Mucosa
Located in Proximal Stomach (80% of secretion).
Secretes:
1) Acid
2) Pepsinogen
3) Intrinsic Factor
4) Mucus
Hirschsprung’s Disease
Congenital megacolon, caused by an absence of Enteric innervation in a segment of the colon. Constriction and loss of coordinated movement of involved segment.
Contents accumulate proximal to constriction, leading to dilation. Severe constipation.
Peptide Forms Proteins Can Be Absorbed As
1) Amino Acids
2) Dipeptides
3) Tripeptides
Larger ones can be absorbed poorly if at all
Hepcidin
Regulates entry of iron into plasma by binding directly to Ferroportin. Causes internalization and degradation of Ferroportin.
Early Phase of Dumping Syndrome
Nausea, vomiting, diarrhea
Function of GIP
Stimulate insulin release from the Pancreas
Bilirubin Glucoronide
Soluble salt. Product of Bilirubin conjugated by Glucoronic Acid in Liver.
Reduce Ferric Iron to Ferrous Iron
1) Vitamin C
2) Citric Acid
3) Duodenal Cytochrome b (Dcytb) – Brush Border Enzyme
Acid Secretion Mechanism: Gastrin
1) Binds to Gastrin/CCK-B receptors on Parietal Cell
2) Activates Phospholipase C
3) Forms IP3
4) Ca2+ released as Second Messenger
Phosphatidic Acid Pathway
Enterocyte processing in starving state. Phosphatidic Acid formed from:
1) two Acyl CoA
2) α-Glycerophosphate
Phosphatidic Acid then reacts with one more Acyl-CoA. Forms:
1) Triglyceride
2) Phosphate
Breakdown products from Amylopectin and Amylose by α-amylases
All oligosaccharides
1) Maltose
2) Maltotriose
3) α-limit dextrins
Triggers of Gastrin Secretion
1) Peptides/amino acids in stomach
2) Distention of stomach
3) Vagal Stimulation (Mediated by GRP)
Absorbs Glucose and Galactose into Enterocyte
Na-Dependent Active Transport System (SGLT-1)
Facilitated diffusion, then, into blood
Intestinointestinal Reflex
Inhibition of contractile activity in more proximal portions of the small intestine to prevent movement of materials into severely distended sections.
Mediated by Extrinsic Nervous System
Pyloric Gland Mucosa
Located in Distal Stomach.
Secretes:
1) Gastrin (mostly)
2) Some mucus and pepsinogen
Location of Somatostatin Release
D Cells throughout GI tract
Reabsorbed and Secreted in Striated Duct (Salivary Glands)
Reabsorbed:
1) Na
2) Cl
Secreted:
1) K
2) HCO3
Location of Secretin Release
Secreted from S Cells of proximal Small Intestine
Function of GRP
Stimulates Gastrin release
Location of GIP Secretion
K Cells in proximal Small Intestine
Function of GI Longitudinal Muscle
Change length
Parietal Cells (Oxyntic Gland)
Secrete Acid and Intrinsic Factor
Pathologies Which Lead to High Protein Concentration in Pancreatic Juice
1) Chronic Pancreatitis
2) Cystic Fibrosis
Gastric emptying mainly controlled by signals from _____
Duodenum
Functional Regions of Gastric Secretion
1) Oxyntic Gland Mucosa (80%)
2) Pyloric Gland Mucosa (20%)
Pernicious Anemia
Anemia resulting from absence of Vit B12
Major Causes of Lipid Malabsorption
1) Failure to Digest
2) Absence of Bile Salts
3) Condition Affects/Decreases Number of Absorbing Cells
4) Failure to Synthesize Apoproteins
Cause of Pigment Gallstone
Bilirubin becomes unconjugated and precipitates with Calcium.
Calcium Bilirubinate
Zollinger-Ellison Syndrome
Overproduction of gastric acid due to gastrin-releasing Gastrinoma
Relationship: Pressure in Proximal Stomach and Gastric Emptying
Inverse.
α-Melanocyte-Stimulating Hormone (α-MSH)
Melanocortin type released from POMC neurons. Binds to Paraventricular Nuclei Neurons (among other nuclei) to reduce eating. Activation of receptor mediate by Paraventricular Nucleus to Nucleus Tractus Solitarus pathway (stimulates sympathetics).
Physiologically-Active Components of Gastric Juice
1) HCl
2) Pepsin
3) Mucus
4) Intrinsic Factor
Result of Excess Iron: Liver
1) Cirrhosis
2) Liver Cancer
Hepatocyte Bile Salt Secretion Pumps
1) ATPase-Dependent Bile Salt Export Pump (BESP)
2) MRP2 (lesser extent)
Endocrine Cells (Oxyntic Gland)
Secrete products regulating gastric function
Functions of Secretin
1) Stimulates bicarbonate and water secretion in Pancreas/Liver
2) Increases Liver Bile Production
3) Inhibits Gastric Acid Secretion
Monitor Peptide
Peptide regulator of CCK release secreted by Pancreas
Phases of Migrating Myoelectric Complexes
Phase I: Quiescent Phase
Phase 2: Small, irregular activity
Phase 3: Regular Activity
Apical Membrane Transporter Secreting Cl into Lumen from Crypt Cell
CFTR Channel
Abetalipoproteinemia
Lipid malabsorption due to inability to synthesize ApoB (component of Chylomicrons).
Absorbed free cholesterol in Enterocytes
Significant portion re-esterified with fatty acids. Some left free. Both transported into Chylomicrons
Lateral Nuclei (Hypothalamus)
Feeding center. Cause hyperphagia when stimulated
Cell Types in Pancreas
1) Acinar Cells
2) Centroacinar Cells
3) Duct Cells
Sphincter of Oddi
Sphincter from Common Bile Duct to Duodenum
Location of Active Reabsorption of Bile Salts
Terminal Ileum
Colipase
Prevents inhibition of pancreatic lipase by bile salts.
Non-enzymatic protein secreted as inactive by pancreas (trypsin activates).
Ghrelin
Orexigenic hormone produced in Stomach and Proximal Small Intestines.
Hiatal Hernia
LES and Stomach move up through Esophageal Hiatus in Diaphragm
Location of Bile Salt Conjugation
Liver
Choleretics
Substances stimulating increased bile secretion
Location of Gastrin Secretion
G Cells in Stomach
Oxyntomodulin (OXM)
Anorexigenic proglucagon-derived peptide. Secreted from Distal intestine in proportion to ingested calories. Short-term action.
Familial Iminoglycinuria
Defect in uptake of proline and hydroxyproline
Fate of Flatus
All except Nitrogen can diffuse through intestinal mucosa to reduce volume.
Breaks heme down to release free iron
Heme Oxygenase
Lecitithins
Primary phospholipid in bile. Improves solubilizing-ability of micelles after itself being solubilized by bile salts.
External Anal Spincter
Prevents defecation. Tonically-contracted
Transports Ferric Iron in Blood
Plasma Transferrin
Location of most water absorption in Large Intestine
Proximal colon
Hepatocyte Transporter Extracting Bile Salts from Portal Blood
Sodium-Taurocholate Cotransporting Peptide (NTCP)
Cephalic Phase (Acid Secretion)
Initiated by thought, sight, taste, or smell of food. Vagus nerve increases acid secretion by:
1) ACh stimulation of Parietal Cells
2) ACh-caused release of GRP
Hartnup Disease
Defect in uptake of neutral amino acids
Monosaccharides absorbed by intestine
1) Glucose
2) Galactose
3) Fructose
Enzymatic Components of Pancreatic Secretion
Secreted in Active Forms:
1) Pancreatic Lipase
2) Pancreatic Amylase
Secreted in Inactive Forms:
1) Trypsin
2) Chymotrypsins
Secreted by Acinar Cells
1) Peptidases
2) Lipases
3) Amylases
Luminal-side Structure of Parietal Cells which enlarges when activated
Canliculus
Stimulator of Pepsin Secretion
Vagal Stimulation
Secondary Bile Acid
Converted by bacteria from Primary Bile Acids in the intestines.
Dumping Syndrome
Lower end of the small intestine fills too quickly with undigested food. Common after stomach surgery
Causes Ileocecal Sphincter to relax
Ileum distention
Function of GI Circular Muscle
Change diameter
Location of VIP Release
Nerves in Mucosa and Smooth Muscle of GI Tract
Primary excretory pathway for cholesterol
Loss of bile salts in feces. Usually equal to dietary input.
Brush Border Peptidases
“Finish the job” started by Endo/Exopeptidases. Breaks further down into oligopeptides and amino acids.
Chief Cells (Oxyntic Gland)
Secrete Pepsinogen
Functions of Serotonin
1) Stimulate Intestinal Fluid and Mucus Secretion
2) Stimulate Gut Motility
Convert Ferrous Iron to Ferric Iron
1) Ferroportin
2) Ferroxidase Hephaestin
Transporter for Active Reabsorption of Bile Salts
Apical Sodium-Dependent Bile Salt Transporter (ASBT)
Trigger of Secretin Release
Released in response to acid
Submucosal Plexus
Network of enteric nervous system found in the intestines. Controls secretion
Proteins in Saliva
1) α-amylase
2) Lingual Lipase
3) Mucin
4) Epidermal/Nerve Growth Factors
