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1
Q

Macronutrients vs. Micronutrients

A

macronutrients: carbohydrates, fats, proteins (amino acids)
micronutrients: vitamins and minerals (electrolytes, magnesium, iron etc)

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2
Q

Internal vs External Environment and Excretion

A

Excretion is removal of cellular waste from body. does not apply to digestion because GI is in external environment.

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3
Q

Actions of the Digestive System

A
  1. Digestion: chemical and mechanical
  2. Absorption: products of digestion brought into body
  3. Secretion: Exocrine secretions include digestive enzymes, water, mucus (protective secretion), bile, acid, bicarbonate (protective).
  4. Motility: progression, mixing and regulating passage.
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4
Q

Peritoneum Function and Structure

A

Functions to suspend the digestive tract organs in the abdominal cavity.

Structure is a thin layer of connective tissue and simple squamous epithelium.
visceral vs. parietal: visceral peritoneum surrounds the organ. parietal peritoneum is along the body wall.

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5
Q

Peritoneal Cavity

A

potential space containing fluid. peritonitis is an infection in the peritoneal cavity caused by a break in peritoneum.

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6
Q

Retroparitoneal

A

Organ is only partially covered by peritoneum. Example is liver

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7
Q

Mesentery

A

where peritoneum is back-to-back with self and functions to suspend organs. It is also the site of a lot of blood vessels and adipose.

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8
Q

Function of gut microbiome

A

small amount of digestion, nutrient extraction. Also release vitamin K. Protective functions include protecting a person from colonization by pathogenic microorganisms by outcompeting. They are also thought to play some kind of role in the development of the immune system.

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9
Q

dysbiosis

A

abnormal gut biome which may lead to disease. Example is C.diff and IBD

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10
Q

Antibiotic-Associated Colitis

A

Antibiotic-associated colitis or C.diff. Pseudomembranous colitis that presents with yellow pseudomembrane patches on the surface of the colon.

Colitis means inflammation of the large intestine.

Treatment: fecal microbiota transplant (FMT) to put good bacteria back into gut.

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11
Q

Inflammatory Bowel Disease (IBD)

A

cause is unknown but may be due to dysbiosis or a genetic component. Researchers have found genes that are linked to IBD and are involved in innate immunity and barrier function. IBD is classified into two categories:

  1. ulcerative colitis: restricted to colon, inflammation in mucosa and continuous lesions.
  2. Crohn’s Disease: inflammation can be anywhere in the GI tract but tends to affect the ileum and anal region. Lesions are transmural (goes through all layers) and discontinuous.

Treatment: anti-inflammatory drugs like glucocorticoids, but if disease is more serious may use biological therapy (anti-TNFalpha).

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12
Q

Tissue Structure of Digestive Tract

A
  1. mucosa: epithelium, lamina propia (MALT), muscularis mucosa.
    - protective: located in esophagus and has high density of MALT
    - secretory: located in stomach and has a lot of glands and is highly folded.
    - absorption: located in small intestine and has a very large surface area and very long length.
  2. submucosa: glands, neurons, blood vessels
  3. muscularis externa: smooth muscle for motility. includes circle muscle, longitudinal muscle and myenteric plexus.
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13
Q

Fiber

A

carbohydrates that are undigestible. Important because get into large intestine and holds water which helps with motility.

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14
Q

Digestion and Absorption of Carbohydrates

A

Digestion:

  1. Oral cavity: salivary amylase breaks down polysaccharides
  2. Stomach: salivary amylase is inactivated by low pH
  3. Small intestine: pancreatic amylase breaks down further but not small enough.
  4. Brush border enzymes break down to small particles necessary for absorption. Examples of brush border enzymes are sucrase, lactase etc…

Absorption:

cotransporter of glucose and sodium powered by the sodium gradient which is maintained by the sodium-potassium ATPase pump.

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15
Q

Digestion and Absorption of Proteins

A

Digestion:

  1. Stomach: pepsin turns proteins into peptides of about 50 AA.
  2. Small intestine: trypsin, chymotrypsin and carboxypeptidase (pancreatic enzyme) and brush border enzymes.

Absorption:

co-transport coupled to sodium. specific transporters for AA’s.

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16
Q

Transcytosis

A

absorption of intact proteins (polypeptides). Mechanism for passive immunity in infants.

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17
Q

Zymogens

A

inactive enzyme precursors.

Pepsinogen –> Pepsin in the stomach. Chief cells secrete pepsinogen. When the structure is modified slightly it acts to promote cleavage by peptidase to form pepsin.

trypsinogen –> trypsin. Cleaved by enterokinase which is a brush border enzyme . Trypsin in turn acts to cleave other pancreatic zymogens. Pancreatitis results from inappropriate activation of enterokinase.

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18
Q

Digestion and Absorption of Fats

A
  1. Emulsification: emulsifying agents are bile salts and phospholipids. Both molecules are amphipathic. Bile salts are synthesized in the liver from cholesterol. Formation of emulsion droplets
  2. Digestion: lipase is bound to emulsion droplets by the amphipathic protein colipase which is secreted by the pancreas.
  3. Micelle formation: Micelles contain fatty acids, monoglycerides, bile salts, phospholipids, cholesterol and fat-soluble vitamins. They function to ferry digested fats to enterocytes.
  4. Absorption: Micelles are constantly breaking apart at reforming. While broken, digested products are now in solution and can diffuse across enterocyte membrane.
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19
Q

Transportation of Digested Fats

A

digested fats are packaged into TAG.

Chylomicrons transport TAG, cholesterol, fat soluble vitamins, phospholipids, apolipoproteins through lacteals into the lymphatic vessels and eventually into the systemic circulation.

TAG is released to monoglycerides and fatty acids for cellular uptake by lipoprotein lipase.

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20
Q

Cholesterol Absorption

A

Absorption occurs in small intestine.

Two sources: cholesterol in the bile from the liver is targeted for elimination from the body and the second source is dietary.

Ezetimibe: drug that blocks the carrier protein for cholesterol in the GI tract, reducing absorption.

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21
Q

Iron Absorption

A

Apical transporter DMT-1 brings iron into enterocyte

Iron can either bind to ferritin (intracellular) or the basolateral transporter ferroportin (transports iron into blood).

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22
Q

Iron Absorption Regulation

A

Regulation of absorption through two routes

  1. from bone marrow: need iron to make blood cells.
  2. from body iron stores: iron is mainly stored in the liver. The liver releases hepcidin (hormone) when iron levels are high. Hepcidin binds to and causes degredation of ferroportin preventing absorption of iron into the bloodstream
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23
Q

Hemochromatosis

A

iron overload most commonly due to a genetic mutation in HFE. Result is unregulated iron absorption leading to free radicals and tissue damage. Liver, pancreas, heart and joints are most sensitive. Recessive. Treatment is phlebotomy.

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24
Q

Vitamin B12 Absorption

A

Associated with metabolic reactions and cell division.

Absorption requires Intrinsic Factor which is a protein produced by parietal cells in the stomach. Intrinsic Factor binds to vitamin B12 to form a complex which travels to the ileum where absorption occurs by receptor-mediated endocytosis.

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25
Pernicious Anemia
lack of intrinsic factor that leads to malabsorption of vitamin B12. Can be caused by autoimmune disease that destroys parietal cells or in Crohn's disease where severe inflammation in the terminal ileum can cause decreased absorption.
26
Celiac Disease
1. inappropriate autoimmune response to gliadin which is a peptide derived from gluten involving CD4+ helper T cells. 2. Also called celiac sprue or gluten sensitive enteropathy. 3. Causes loss of surface area and intestinal villi as well as inflammation and tissue damage to small intestine. 4. Decreases iron (absorbed in duodenum) and folate absorption which may lead to anemia. 5. Treatment: eliminate gluten from diet. Therapies currently being researched include digestive enzymes and methods to decrease intestinal permeability.
27
Adjustable Gastric Banding
Bariatric Surgery. band around fundus to create a small pouch at the top of the stomach so patient feels full quicker. Restrictive procedure.
28
Roux-en-Y
1. gastric bypass that combines restrictive and malabsorption through anatomical rearrangement. Still create pouch at the fundus to restrict food intake but then you bypass the upper small intestine by connecting a piece lower down to the stomach. Formation of "Y". 2. Alimentary channel: channel where food goes from stomach to lower small intestine. 3. Biliopancreal channel: duodenum portion of small intestine that still produces/carries secretions. 4. treatment for type II DM because of weight loss and endocrine alterations. Thought that the upper GI may influence glucose homeostasis. And, in the lower small intestine L-cells release GLP-1 and PYY faster because food reaches this area quicker. 5. Requires post-operation micronutrient supplementation because of iron deficiency.
29
Enteric Nervous System (regulation of GI tract)
- myenteric plexus between layers of smooth muscle and submucosa plexus. - afferent neurons: chemical sensors, stretch sensors - efferent neurons: secretory cells, smooth muscle - interneurons: connecting and coordinating. - Big input from parasympathetic nervous system by preganglionic neurons in the vagus nerve. However, they can operate in isolation.
30
Pacemaker Cells
specialized cells in smooth muscle that are spontaneously active which means there is electrical activity without nervous system input. Electrical coupling occurs in groups via gap junctions. Responsible for slow wave electrical activity
31
Smooth Muscle Electrical Activity
1. slow waves: basic electrical rhythm (BER). Generated by pacemaker cells. Stomach is 3/min. Duodenum 12/min and Ileum 9/min. Determines frequency of contraction. 2. Action potentials: spikes where depolarization is high enough to open calcium channels and let calcium into the cell. Calcium regulates muscle contraction. The amount of calcium determines the strength of contraction
32
GI Hormones and Paracrine
Hormones are released by endocrine cells in the epithelium and into the blood stream. Important hormones include gastrin, cholecystokinin (CKK), secretin, incretins (GLP-1 and GIP). Paracrine are released and act on neighboring cells. Important paracrine are histamine, somatostatin, serotonin.
33
Phases of GI control
Phase refers to the location of the stimulus Cephalic Phase: stimuli are in the mouth. Examples are seeing food, smelling food, chewing and emotional states about food. Gastric Phase: Stimuli are presence of peptides. Examples are stomach distention, and acid secretion. Intestinal Phase: Stimuli are distention, acidity and presence of digested products.
34
Salivation in GI regulation
amylase is released in response to food in the mouth and it digests carbohydrates.
35
Swallowing in GI regulation
1. Buccal (oral) phase: Part of the voluntary initiation. When food is in the mouth, you retract the tongue which pushes food to the pharynx. The soft palate elevates to prevent food from going up into the nose. This stimulates pharyngeal sensory receptors that coordinate the rest of the swallowing behavior. 2. Pharyngeal Phase: Food is directed to the esophagus. Respiration is inhibited and the glottis is closed. The larynx elevates which closes the epiglottis. 3. Esophageal Phase: Food is moved from the esophagus to the stomach by peristalsis. The esophageal sphincter relaxes.
36
Vomiting
Technical term is Emesis. Completely separate behavior controlled by separate nuclei, from swallowing. Stimuli: 1. Irritant in the GI tract: Increase serotonin secretion which activates afferent neurons in the vagus nerve which then activates the vomiting center. 2. Toxic Substance in the Circulation: Acts on an area in the brainstem called the postrema which is posterior to the 4th ventricle and is outside the blood brain barrier. This activates the vomiting center. 3. CNS stimuli: Example is a vestibular mismatch
37
Anti-Emetics
serotonin antagonists: Zofran. Binds to 5-HT3 serotonin receptor antagonistically Substance P antagonists: aprepitant (Emend). Mechanism unknown.
38
Heartburn
Lower Esophageal Sphincter (LES) normally prevents gastric reflux. GERD = gastroesophageal reflux disorder. Causes: - lack of tone in LES - increases in abdominal pressure. Examples are overweight, pregnancy, large meals - Hiatal hernia: Occurs when a little part of the fundus slips up through the hiatis (hole in the diaphragm for the stomach).
39
Barret's Esophagus
occurs as a result of GERD Results in intestinal metaplasia: simple columnar epithelium, villi and goblet cells present in the esophagus which you should never see. Has an increased risk for esophageal adenocarcinoma (rare form of cancer) Treatment: anti-secretory drugs that block acid secretion.
40
GI control Stomach: Secretion of Acid
Translocation of proton pumps (H+/K+ ATPase) to the apical plasma membrane in parietal cells. Release HCl.
41
Regulation of Gastric Acid Secretion
1. Positive regulators: increase the translocation of proton pumps therefore increasing acidity. - gastrin: hormone released by G cell. Released by Gastric Phase stimuli - histamine: paracrine released by ECL cells which is stimulated by G cell in gastric phase. - ACh: Nt released by enteric neurons due to cephalic phase stimuli 2. Negative regulator: somatostatin which is released in response to increased HCl in the stomach.
42
Inhibitory Feedback from intestine in regulation of Gastric acid secretion
Function to prevent too much acidic chyme dumped into duodenum. Enterogastrins include CCK, secretin, GLP-1 and GIP. Decrease acid secretion.
43
Peptic Ulcer Disease
lesions in the mucosa in the stomach or duodenum. Causes: NSAIDs and H.pylori
44
H.pylori
burrows into mucosa to escape acidic environment and also produces urease which buffers the acid in the immediate surroundings. Results in chronic gastritis (inflammation of the stomach lining), and production of cytokines 1. Ulcer in the pyloric region: characterized by the development of a duodenal ulcer. G cells are stimulated to secrete more gastrin while somatostatin is inhibited. Gastrin stimulates parietal cell proliferation ultimately leading to acid hyper-secretion. 2. Ulcer in the body of the stomach: characterized by atrophic gastritis. Leads to hypochlorhydria (hyposecretion of acid). Results in the development of a gastric ulcer which is a significant risk factor for gastric cancer with intestinal metaplasia (columnar epithelium, villi and goblet cells).
45
Drugs that reduce acid secretion
Histamine Blockers: Histamine antagonist that blocks the release of histamine by ECL cells. Proton pump inhibitors: bind to and inactivate the proton pump in the parietal cell.
46
Gastric Motility
1. Receptive relaxation: as you are eating your stomach relaxes. 2. peristalsis: stretching of the stomach triggers peristalsis. Rate is determined by BER and is 3/min in the stomach. 3. stomach emptying: - Gastric phase stimuli (stomach distention and/or gastrin) increases strength of contractions and increases stomach emptying. - Intestinal phase stimuli decreases the strength of contractions and slows stomach emptying. 4. enterogastrones: inhibit acid secretion and inhibit smooth muscle. No change in slow waves (affects the rate/timing of contractions), just the strength of the contractions.
47
Pancreatic Cell types
acinar cells secrete digestive enzymes and duct cells secret bicarbonate and fluid.
48
Pancreatic Regulation
Hormone regulation secretin: released by endocrine cells. Release is stimulated by low pH. Functions to act on duct cells to promote excretion of bicarbonate and fluid. CCK: release is stimulated by the presence of fats and peptides. Functions to stimulate acinar cells to secrete digestive enzymes. Also have stimulation from cephalic and gastric phases via the vagus nerve.
49
Bile
composed off bile salts, phospholipids, bicarbonate, cholesterol, bile pigments, trace metals.
50
Sphincter of Oddi
Sphincter of Oddi: determines whether bile is secreted into duodenum or put back into gall bladder Interdigestive Period: Sphincter of Oddi is contracted which causes bile to flow into gall bladder for storage. Digestive Period: Sphincter of Oddi is relaxed and bile is released into the duodenum
51
Hormone Regulation of Bile
Secretin: stimulates duct cells. CCK: triggers contractions and causes relaxation of sphincter of Oddi
52
Enterohepatic Circulation
Function: recycle bile salts Flow: bile flows into the intestines and specific transporters take up bile salts from the ileum and into intestinal capillaries which transport them back to the liver. Gallstones when cholesterol precepitates
53
Gallstones
Too much cholesterol in the gall bladder which will precipitate out. Bile salts keep cholesterol soluble to prevent precipitation. 1. Gallstone in cystic bile duct: painful gallbladder contractions 2. Gallstones blocking common bile duct: pain, nausea, lack of bile release, failure to release bilirubin leading to jaundice. 3. Gallstone blocking duodenal papilla: inappropriate activation of pancreatic zymogens and acute pancreatitis. Blocks the release of bile and digestive enzymes from pancreas. Treatment: cholecystectomy (removal of gallbladder), ERCP (endoscopic and put dye to determine where the stones are), non-surgical (addition of bile salts to solubilize stone)
54
Small Intestine Cell Types
Crypt cells secrete fluid to help maintain solubility and aid in absorption. Villi cells function in absorption.
55
CFTR Transporter in Small intestine
Rate limiting step of secretion is apical membrane chloride channel. CFTR transporter. Associated with Cystic Fibrosis intestinal blockage: usually happens with infants and due to lack of secretion from CFTR. pancreatic insufficiency: happens if lack of secretion from CFTR is very severe. With too much secretion get watery diarrhea. This occurs in cholera
56
Movements of the Small Intestine
segmentation: occurs during digestive period and is turned on by cephalic phase stimuli. Alternation of smooth muscle contractions and relaxation. BER in duodenum is 12/min and gradually decreases to 9/min in ileum. Allows for net movement toward cecum. During interdigestive period: migrating motor complex "sweeps" out small intestine.
57
Function of Large Intestine
absorption of fluid, secretion of mucus, bacterial digestion, storage of feces, defecation.
58
Motility of Large Intestine
mixing movement: slow, irregular contractions of circular muscle mass movement: propulsive movement through sustained contraction of circular muscle that provides a stimulus for defecation.
59
Muscles and sphincters in defacation
internal anal sphincter (smooth muscle): innervated by enteric neurons external anal sphincter (skeletal muscle): innervated by somatic efferent neurons puborectalis: muscle that creates a more acute angle between the rectum and the anus to keep things from leaking out. During defecation have conscious relaxation of skeletal muscle.
60
Sequence of defecation
1. mass movement 2. defecation reflex: stimulus is distension of rectum and result is contraction in rectum, relaxation of internal anal sphincter and contraction of external anal sphincter 3. increased pressure in rectum (urge to defecate) - When you want to delay: contraction of external anal sphincter, contraction of puborectalis, reverse peristalsis - Ready to defecate: relaxation of external anal sphincter, relaxation of puborectalis muscle, forward peristalsis, Valsalva maneuver (conscious pushing to increase abdominal pressure)
61
Sources of Blood Flow to Liver
common hepatic artery from aorta and the hepatic portal vein
62
Hepatocyte Functions
1. produce bile 2. nutrient homeostasis: in the absorptive state synthesize glycogen and TAG. in the post absorptive state have glycogenolysis, gluconeogenesis, ketogenesis 3. biotransformation: metabolism of drugs, hormones etc to promote excretion via the urine 4. synthesis of plasma proteins: albumin binding proteins, clotting factors, complement 5. cholesterol homeostasis
63
Cell Types in Liver (excluding hepatocytes)
1. Endothelial cells: located in the sinusoid. They have no basement membrane and have gaps between cells. 2. Canaliculus: spaces between hepatocytes. 3. Kupffer cells: macrophages, involved in iron recycling 4. Stellate cells (Ito cells): connective tissue cells. Stimulated in chronic liver injury to form more connective tissue. Too much connective tissue is called fibrosis. Cirrhosis is the terminal phase of fibrosis where connective tissue isolates islands of hepatocytes.
64
LDL, VLDL, HDL
VLDL: TAG rich and made by liver from extra glucose. Sent to cells and TAG is extracted by lipoprotein lipase. LDL: Function is to deliver cholesterol to cells. Uptake of cholesterol is by receptor mediated endocytosis. HDL: reverse cholesterol transport. Begins with very little TAG but has the capacity to travel around and scavenge for excess cholesterol around the body to bring back to the liver.
65
Risk for Atherosclerosis
Risk for atherosclerosis with higher levels of LDL and lower levels of HDL familial hypercholesterolemia: major cause is a mutation in the gene for the LDL receptor.
66
Liver Role with Cholesterol
1. synthesizes cholesterol: HMG-CoA reductase. 2. synthesis of HDL 3. Uptake of LDL: regulates levels of cholesterol in the circulation 4. synthesis of bile salts 5. secretion of cholesterol into bile: eliminate from the body
67
Dyslipidemia Treatments
Statins: inhibit HMG-CoA reductase, reduce LDL cholesterol Ezetimibe: block cholesterol absorption in small intestine, reduces LDL Increasing HDL : niacin and fibrates.
68
Hematochezia
Bright red blood in stool. Usually due to inflammation in left colon
69
Melena
Passage of tarry stools usually associated with upper GI bleeding.
70
Treatment for ulcerative colitis
5-aminosalicylate (5-ASA) absorbed in large intestine.
71
infliximab
TNF-alpha treatment for IBD
72
dermatitis herpetiformis
skin rash from celiac disease.
73
zonulin
regulatory molecule that causes tight junctions to open up. stimulated by gluten peptides.
74
dysplasia
seen in Barret's esophagus. Cellular abnormalties that indicate the beginnings of malignant transformation.

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