Professional Documents
Culture Documents
GI PHYSIOLOGY 3-14-11
- GI provides nutrients to body through motility, secretion of digestive juices, digestion, absorption, and excretion of wastes. (Highlighted + Blood flow
are controlled processes)
- Nutrient: Substance found in food used by the body for growth, repair, and maintenance. Water, minerals, monosaccharides, fats, AAs, vitamins.
- Consume ~ 2000 g/day, Excrete ~ 200-400g/day.
- Feces 75% H2O, 25% Solids. Solids = 30% dead bacteria and 30% roughage.
- Brown color of poo is from bilirubin. Smell is from bacteria of colon and food we eat.
- Water: Consume 1500ml/day, but 7000ml is secreted into the lumen/day (from salivary glands, stomach, etc.) 8500ml/day total. 8300 is absorbed in
small and large intestine. 200 is in poo.
- Motility: Contraction/relaxation of sphincters 7 of them. Upper and lower esophageal, Pyloric, Oddi, Ileocecal, Internal and External anal.
o Resting State: Pressure of sphincter > adjacent segments.
o Relaxed: Pressure = Adjacent segments, permits forward flow.
o Contracted: Pressure of sphincter >> adjacent segments to prevent retrograde flow.
- Phases of Control of Processes
o Cephalic Phase: Initiated when receptors in head are stimulated by Sight, smell, taste, chewing,
through food, and emotional states. Stimuli trigger secretory and contractile responses in GI
tract mediated by ANS (PNS and SNS) modulation of enteric nervous system( ENS) activity.
o Gastric Phase: Initiated by stimuli in stomach (distention, acidity, AAs, peptides). Stimuli trigger
secretory and contractile responses in GI tract mediated by short and long neural reflexes and
by the hormone gastrin.
o Intestinal Phase: Initiated by stimuli in the small intestine. Triggers secretory and contractile
responses in GI tract mediated by short and long neural reflexes and by release of the small
intestine hormones secretin, CK, GIP, GLP-1.
- Receptors in the GI tract: Mechano (stretch, tension, length), Chemo
(acid, osmotic, AA, lipid, glucose), Thermo (purpose is for regulation of
body temperature), and ?Pain?.
- Mechanisms of Communication to Mediate Responses in the GI Tract:
o Endocrine: Relatively slow.
o Neurocrine: Rapid control. Sensory neuron in the wall of the GI
tract. Go to a secretomotor neuron which may stimulate muscles
to contract or glands to secrete things (mucous, serous). Ach and
Substance P are STIMULATORY. NO & VIP are INHIBITORY.
o Paracrine: Intermediate in speed. Control of adjacent cells
actions.
- Saliva has higher K+ and HCO3- and lower Na+ & Cl- than serum. (More potassium, less salt). This is how these things are absorbed/secreted.
- Functions of Saliva:
o Disrupt food particles
o Aid in formation of food bolus for swallowing
o Initiate starch and lipid digestion
o Facilitate taste
o Clean mouth / Bactericidal
o Maintain pH, neutralize lactic acid.
- Secretions of Salivary Glands:
o Mucin Lubrication
o Amylase Starch digestion (Seen in parotid)
o Lipase Fat digestion (Seen in von Ebner glands)
o Lysozyme Antibacterial
o IgA Immune protection
o Growth factor Wound healing.
- As flow rate increases, tonicity will increase with K+ and HCO3-.
- Regulation of Salivation:
o Excited by taste and tactile stimulation from the tongue and mouth (sour taste and smooth objects especially)
o Excited by sight, smell, taste of food.
o Autonomic control from salivatory nuclei located at the junction of the medulla and pons. PNS and SNS are both stimulatory.
- Swallow Reflex:
o Moves food bolus to stomach.
o Tongue pushes bolus to back of mouth.
o Uvula and soft palate push back to keep food from entering nasal cavity.
o Epiglottis and lifting trachea keeps bolus from entering trachea.
o Upper esophageal sphincter relaxes to allow food through.
- Phases of Swallowing:
o Oral: Voluntary initiation
o Pharyngeal: Involuntary Pharynx to esophagus
o Esophageal: Involuntary Esophagus to stomach.
Primary Peristalsis: Continuation of the peristaltic wave from the pharynx (8-10s)
Secondary Peristalsis: Generated by ENS by esophageal distention or irritation.
Receptive relaxation: Both LES and stomach relax prior to the constrictive wave of peristalsis to let food into stomach.
- Neural Control of the Swallow Reflex:
o Sensory CN V, IX, X (Afferent)
o Signal goes to swallowing center in medulla
o Motor V, VII, IX, X, XII (Efferent)
- Peristalsis:
o Ach Constricted portion of food bolus wave
o NO/VIP Relaxed portion of food bolus wave
- Upper 1/3 of esophagus is skeletal muscle controlled
- Lower 2/3 of esophagus is ENS muscle controlled
- By the time the bolus reaches the stomach, amylase from the SGs have already started to work, so some starch, and monosaccarides and disaccharides
are entering.
- Bolus in, small particles out.
- Ionic concentrations are different in the gastric juice (High H+, High Cl-, High K+, low Na+)
- Only particles less than 2mm will be allowed to exit the stomach through the pyloric sphincter.
- Prolonged vomiting = Alkalosis from loss of H+, Hypokalemia from loss of K+, Hypochloremia from loss of Cl-, Dehydration
Stomach Cell Secretions
Secretion Cell Source Functions Other
Mucus Mucus Neck Lubrication Ach stimulates release.
Cells Impermeable to Pepsin.
HCO3- Surface Cells Protection of esophagus / duodenum against acid
Trefoil Protection
Peptides
H+ (from HCl) Parietal / Activates pepsinogen Pepsin Ach stimulates release of H+ via M-3 receptor.
Oxyntic Cells Stimulates Somatostatin Release to inhibit meal-stimulated
gastrin-secretion. Concentration high before meal. Decreases as the
Inhibited by stimuli of the small intestine (secretin, CCK) stomach fills, then rises again as it empties.
Stimulated by Vagal Efferents from the Dorsal Vagal Complex
during cephalic and gastric phases of digestion. Cells will secrete MORE with meals (even though
[H+] is falling)
In Parietal Cell:
CO2 + H2O via CA H2CO3 HCO3 + H+ H+ transported into Gastric Proton Pump: Located in apical
duct of gastric gland, HCO3 goes to bloodstream Anion membrane. Luminal surface exposed to very low
exchange protein trades HCO3 for Cl- Cl- goes with H+ to pH. Unique target for anti-secretory drugs
stomach Some K+ counter-transported in exchange for H+ Inhibition blocks basal and stimulated acid secretion.
Intrinsic ESSENTIAL SUBSTANCE
Factor Binding of cobalamin (Vitamine B12)
Pepsinogen Chief Cells Optimally active at low pH Oligopeptides stimulate further gastrin secretion.
Protein digestion (Protein Oligopeptides)
Gastric Lipase TG digestion
Gastrin G-cells Regulation of acid secretion (H+) via CCKB receptor 17 & 34 AA forms. 34AA is predominant in basal
(Endocrine Stimulates Histamine secretion as well. state, 17 predominant after meal.
cells) Inhibited by somatostatin.
Stimulated by Vagal Efferents from the Dorsal Vagal Complex
during cephalic and gastric phases of digestion
Histamine Paracrine Acts in paracrine fashion on Parietal Cells to release more
secreting cell H+ via H2 receptor
Somatostatin D-Cells Paracrine in nature
- Three Gastric Motor Responses During the Gastric Phase:
o 1. Receptive Relaxation Relaxation of the fundus and body to accommodate volume of meal
o 2. Mixing and grinding Antral peristalsis to grind the meal into small particles and mix with secretions
o 3. Emptying Coordination of antro-pyloro-duodenal motor activity for regulation of gastric emptying. Regulation of fundus tone. This is
controlled so the small intestine is not overloaded by volume and composition of stomach and intestinal contents. The stimuli affect stomach
muscle tone, frequency and strength of antral peristalsis, pyloric resistance to flow (pyloric motility), and intraduodenal pressure and resistance.
- Short neural reflexes go straight from GI organ to GI organ. (Enteric neurons)
- Long neural reflexes go from GI organ to the brain, which then directs another or the same GI organ. (CNS)
- Enterogastrones: A secretion from the duodenum that effect gastric emptying. CCK, Secretin, GIP, PYY, and GLP-1 will inhibit gastric emptying when the
duodenum is full.
- Nutrients in the duodenum will increase the amplitude of the duodenums contractions (More resistance gastric emptying)
- Particle size makes a difference in stomach emptying: Glucose solution or homogenized (grinded up, sludgy) liver will pass almost immediately.
Digestible cubes need more time. Undigestible spheres bigger than 2mm will not pass through until all digestible contents have already passed.
- Fastest rate of emptying occurs when OSMOLARITY OF SUBSTANCE IS EQUAL TO THAT OF PLASMA. (Isosmotic)
- Low pH of stomach contents slows gastric emptying of liquids. (Again, more towards neutral (7), will = faster emptying).
- Gastric emptying of caloric FLUIDS is LINEAR and slower than saline. (Remember, particle size is what limits solid meals)
- The pancreas doesnt auto-digest because the enzymes that attach membranes are stored as inactive precursors and are stored within membrane-
bound granules. These granules have trypsin-inhibitors
- Cephalic and gastric phase stimuli increase pancreatic secretions through PNS mechanisms. Intestinal phase stimuli arising during chyme digestion
have greater effect on exocrine pancreatic secretions, mediated mostly by CCK.
Duodenal Secretions
Secretion Type Functions Other
Secretin Duodenal Stimulates duct cells of pancreas to secrete HCO3 Theory: Secretin binds to a receptor and facilitates
cell Works best in conjunction with Ach or CCK. Alone, output of Cl-, so the gradient is larger for HCO3- to
secretions neither of these two things will result in the same be exchanged for it.
amount of bicarb released.
Stimulates Bile Secretion
Cholecystokinin with CCK-RP and Monitor Peptide In presence of meal protein, Trypsin is busy with
with Trypsin (degrades above products) meal and will degrade less CCK-RP and Monitor
Stimulates pancreatic enzyme secretion peptide
Stimulates Gallbladder contraction (Ach) and
sphincter of Oddi relaxation (VIP/NO) via neural and
humoral pathways.
With Secretin HCO3 from pancreatic duct cells.
Pancreatic Acinar Cell Secretions
(Duct cells of pancreas release Bicarb Bicarb, volume with flow)
Secretion of all Acinar Secretions with VIP, GRP, Ach (Vago-Vagal reflex)
Secretion of Acinar Secretions with CCK
Secretion Type Functions Other
Trypsinogen Proteases Trypsinogen Trypsin via Enterokinase which is
Comprise secreted at the brush border of the duodenum.
Chymotrypsinogen most of
Proelastase human
Procarboxypeptidase A pancreatic
Procarboxypeptidase B enzymes.
Amylase Amyolytic An endoglycosidase. Breaks down starch into products
enzyme which cant be absorbed. Small intestine finishes the job.
Lipase Lipases
Lipase-related proteins
Phospholipase A1, A2
Nonspecific Esterase
Sugars
- Sucrase, glucoamylase, and lactase are embedded in the brush-border membrane to break down sucrose, glucose oligomers, and lactose,
respectively.
- Glucose and galactose require active transport to enter cells (SGLT-1 transporter)
- Fructose is passively absorbed through the GLUT-5 transporter.
- GLUT-2 then transports all of these to the blood.
- Glucose is absorbed completely along small intestine. Lactose absorption varies per individual.
Proteins
- Protein transport
o ALL absorbed through active processes.
o All powered via the Na+/K+ ATPase.
o There are at least 5 transporters, each with a
specific group of AAs they transport.
o Majority absorbed in duodenum, but doesnt get
*completely* absorbed (as compared to glucose
which is completely absorbed).
Fats
Calcium
Note water and Cl- transports above. Also note Cholera toxin, how it
stimulates Cl- to be transferred, therefore Na+, therefore H2O into the lumen.
- Same as above, however colon is also affected by Aldosterone which increases Na+ absorption and therefore H2O absorption.
Colonic Secretion
- Largely mucous and some bicarb. Stimulated by local reflexes and sacral nerves. Protects the mucosa against excoritation, bacteria, and acids, and also
provides an adherent medium for feces.
Fiber
- Swallowed air
- H+ + HCO3 CO2
- Bacterial fermentation
GI Smooth Muscle
- Muscle bundles electrically connected via gap junctions which ensure that muscles will all
depolarize at the same time (as a syncytium).
- Levels of control:
o Myogenic Control
Basic Electrical Rhythm = BER = Slow waves
Slow waves propagated across the gap junctions away from the mouth anus
Stomach 3/min
Small intestine 18/min
Colon 6/min
Frequency of contractions are limited by the frequencies of these slow waves.
Interstitial Cells of Cajal: Pacemakers of Electrical slow waves.
More action potentials in a row = Stronger contraction.
Slow wave depolarization would STILL occur without hormones
o Neurogenic Control
Intrinsic Neural Control
VIP and NO Hyperpolarization. Inhibitory. probability of action potentials going through
Substance P and Ach Depolarization. Stimulatory.
Extrinsic Neural Control
Sympathetic Control Major direct effect of NE is to inhibit the ENS
o Endocrine / Hormonal Control
Gastrin Stimulates gastric motility
CCK Contracts gallbladder, relaxes sphincter of Oddi, slows gastric emptying, enhances intestinal motility
Motilin Stimulated intestinal motility, speeds gastric emptying
PYY Slows gastric emptying, inhibits motility
Neurotensin Slows gastric emptying
- Segmentation Contractions (digestive phase)
o Mix chyme with digestion juices and bring chyme in contact with intestinal wall.
o Food intake and presence stimulate contractions
o Enteric nervous system controls these contractions via inhibitory motor neurons which facilitate the receiving segments to relax so food can
enter them.
- Migrating Motility Complex (MMC)
o After most of a meal has been absorbed, a wave of strong peristaltic contractions (the MMC) arises in the stomach and moves along the small
intestine to the end of the ileum. A new MMC begins in the stomach about every 2 hours between meals
o Function Moves undigested material into large intestine and prevents bacteria from remaining in small intestine long enough to grow and
multiply.
o The MMC is sufficient to move particles larger than 2mm out of the stomach and into the intestines.
o Motilin MMC
- Peristaltic Contractions
o Receiving Segment = Contracted longitudinal muscle
(shortens) and relaxation of the circular muscle (widens)
o Propulsive segment = Relaxed longitudinal muscle
(lengthens) and contracted circular muscle (narrows)
o Reflexive control by ENS.
- Intestino-intestinal Reflex
o Stimulated by large distentions of the small intestine,
injury to the intestinal wall, or various bacterial infections.
o Result complete cessation of intestinal motility
- Gastroileal reflex
o Stimulated by gastric emptying of chyme
o Result Increase in segmentation activity in ileum. Ileal
contents move into large intestine.
- Ileocecal Sphincter Control
o Distention of ileum = relaxation of sphincter.
o Distension of colon = Greater contraction of sphincter.
- Normal Colonic Function
o Absorption of water and ions. Bacterial fermentation of
nonabsorbed nutrients. Storage & elimination of waste and indigestible
materials.
o Cecum Anus = 56-58 hours
o Normal stools range from 3x/day to 1x/3days.
Left-Sided Colon Loop rotates 90 CCW, but doesnt rotate Entire colon on left side.
the rest of the 180 degrees.
Reversed Rotation of Loop rotates 90 CCW, but 180 Clockwise.
Gut Loop (Net is 90 CW). Duodenum is anterior to
and crosses over the transverse colon
Obstruction.
Persistence of Can be ligament, Ligament or fistula Structure for gut
Vitelline duct fistula, or loop to twist around volvulus
diverticulum (obstruction and death of bowel)
(Meckels).
Stenosis of gut Vacuolization of the gut lumen doesnt fully
complete. Stenosis can cause obstruction.
Atresia of gut Lack of blood supply to part of the gut can
cause it to not form Obstruction
Omphalocele Guts coming out of Gut loops go out into the coelom and fail to Intestines inside the DX: US
the umbilical ring. return on the 10th week, or they could umbilical cord. Bowel incidence other anomalies.
rerupture after that. looks normal (protected)
Gastroschisis Guts coming out of Same as omphalocele, but through a Always on the right side of Usually an isolated defect
a rupture to the rupture, not through a structure already the umbilical cord. No other anomalies.
side of the there. Intestines OUTSIDE of DX: US
umbilical ring. umbilical cord. Sick bowel
when baby is born.
Gastrointestinal Histology
Tissue Location Functions Clinical Findings LOOK/Other
Dorsal Surface of Anterior 2/3 Taste. Wet Filiform papillae : keratinized wet, stratified
the Tongue of tongue. willies. squamous epithelium.
Flush out Fungiform papillae: has taste buds embedded in
tasted the epithelium
substances. Circumvallate papillae: Has taste buds along the
lateral margin of the papillae and salivary glands.
Folliate papillae: Along the sides of the tongue.
Taste bud Your face. Duhr. Sensory Cells, Supporting Cells (long cells
projecting up to taste pore), and Stem Cells (at the
base)
Tooth Your moms Crown is part thats showing. Covered with
face. Enamel (formed by layer of cells only present at
time of formation. Thus, all the enamel you see is
all you will ever have in your LIFE).
Dentin layer is below the enamel and is
regenerated throughout life.
Root is embedded in the gums/mandible. Has
Cementum on surface which is what roots it inside
the body.
Ligaments extend from the jaw and to the
cementum.
Central Canal has vessels and nerves. Inside lining
has odontoblasts.
Alveolar Ridge aka Gums. Barrier to Junction where it meets the tooth is the barrier.
infections.
Salivary Glands Tubulo- Lubrication Mucus secreting cells (mostly seen in a tubular
alveolar for foods. fashion) Seen a lot in sublingual and buccal
gland found in Serous secreting cells (mostly in an alveolar
places where configuration). Seen a lot in parotid (amylase) and
yousalivate von Ebner (lipase)
Composite cells: Secrete both mucus and serous
fluid. Seen in submandibular.
Myoepithelial cells on the outside of the tubulo-
alveolar parts to squeeze stuff out.
Gastrointestinal Histology
Tissue Location Functions Clinical Findings LOOK/Other
Gut Tube Esophagus Lumen lined by simple columnar
down to epithelium (ONLY ENDODERMAL PORTION.
Rectum EVERYTHING ELSE IS MESODERM).
After lumen, there is lamina propria (loose
connective tissue).
Then, muscularis mucosa.
Then, submucosal layer
Then, muscularis (inner circular layer, then
longitudinal layer)
Then, serosa in intraperitoneal regions or
adventitia if region is retroperitoneal.
Mucosal layer = lumen + lamina propria +
muscularis mucosa
Esophagus Push the food Contains submucosal ganglia. No serosa.
from the mouth Mucus secretors, and ONLY MUCOUS.
down to the
stomach.
There is not much connective tissue along the face of each hex side, but there is some
surrounding each triad.
3 Liver Models:
1. Hepatic Lobule (like talked about above)
2. Portal Lobule (Bile drains away from 3 different central veins)
3. Portal Acinus (Seeing that arterial blood will go from outwards in towards
central vein. So bad stuff will happen to the outside first. Outward cells work more
with oxygen (get more arterial blood), and central will work more in glycolysis and
FA synthesizing)
Bile Duct Simple cuboidal epithelium
As the duct gives way to hepatocytes, the spot is called Herrings Canal.
Hepatocyte SER and Cytosol Carb (glucose) metabolism Bilirubin is conjugated with glucouronic acid
SER Make bile, metabolizes lipid-soluble drugs and steroids and bilirubin in the hepatocytes so it can then be eliminated.
RER and Golgi Make serum proteins in blood
RER, Golgi, SER Lipoprotein synthesis
Mitochondria Urea formation
Hepatocytes secrete bile into the bile canaliculi [spaces between hepatocytes]
which then filters into Herrings Canal, then to bile duct.
Hepatocytes secrete other material into the Space of Disse (space between
hepatocytes and sinusoid. Mostly empty in healthy liver)
Sinusoids Allow material to pass: Hepatocytes Space of Disse Sinusoid Body
Kupffer cells hang out here to nom things.
Exocrine Makes enzymes necessary for digestion. Duct system penetrates into the secretory
Pancreas portion. These duct cells are called centroacinar cells.
Duodenal Submucosal / Brunners Glands: Secretes HCO3. They are BELOW THE
SUBMUCOSA. (In pylorus, all goblet cells are above the mucosa)
Functions: Lipid processing. Break them down via Lipases (surround masses of TGs
FAs and glycerol). FA combine with bile salts (emulsifiers) Micelles. Micelles
Surface epithelium of intestine enter enterocyte SER reassembles TGs
Conversion to Chylomicrons Transfer to space between enterocytes Lymph
vessels Liver for further processing.
Intestinal Capillary bed is at the core of the villus embedded in lamina propria with arteries
Vasculature lining, and veins at the middle, running out.
Lacteal (lymph vessel) is also at the center, where the chylomicrons migrate to. Can
be identified because of lack of RBCs.
Meisners / Located in the submucosal layer
Submucosal
Plexii & Ganglia
Auerbachs / Located between the circular and longitudinal muscle layers.
Myenteric Carries PNS, SNS, and sensory fibers.
Ganglia
Gut Associated Recognizes antigens and clones lymphocytes to react against detected antigen.
Lymphoid Monitoring: Intraepithelial lymphocytes which hang out between enterocytes to
Tissue (GALT) check for stuff. Also, M-Cells which are special cells that sample lumen material in
pockets to expose it to lymphocytes.
M-cells are mostly in the ileum in places called Peyers Patches Lots of
lymphoid nodules filled with B-Cells and T-Cells. This induces IgA secretion into
the lumen
Large Intestine More goblet cells, less enterocytes.
Tenia coli Ridge along the middle of the intestine
Further down colon = More mucous cells.
No Peyers Patches, but will see several plasma cells in the lamina propria.
Appendix Lots of lymph nodules, as in the ileum
Anorectal Pectinate Line.
junction
Lip Outer layer is keratinized stratified squamous epithelium
transition
Inner is wet stratified squamous epithelium
Serous glands within.
Oral Cavity Lesions & Disorders
- Most important area of pathology is the alveolar (gum) ridge.
Name Causes Pathogenesis Clinical Diagnosis/Treatment/Other
Dental Caries / Most common chronic childhood Untreated = Pain, infection, Prevention: Fluoride incorporates
Tooth Decay / disease. in older adults. lost productivity, tooth loss. into crystalline structure, resistant
Cavities to bacterial acids.
Meth Mouth = Meth use
potentiating cavities.
Periodontal Disease Tobacco use. Inflammatory response to Destruction of: Alveolar
Increased prevalence in bacterial pathogens Host bone, root cementum,
diabetics. immune response Presence of PDL (attachment) fibers.
calcified bacterial deposits
Ultimately tooth loss.
Pyogenic Granuloma Early phase of irritation 75% on gums, also tongue, lower Smooth, lobulated red
fibroma. lip, BM. mass. Usually
pedunculated.
Trauma More common in children
because theyll chew on their
Also pregnant women. mouth.
Primary HSV HSV-1 (genital HSV-2) Physical contact transmission. Mostly seen inside lip.
Primary Heprpetic 1st infection with HSV.
Gingivostomatitis Mostly young children.
Esophageal Chronic reflux and damage from Striking increase in these Pain, difficulty swallowing,
Adenocarcinoma acid. Usually preceded by cancers recently. weight loss, hematemesis,
Barretts Esophagus. of all esophageal cancer in vomiting, chest pain.
US. (Most common US Most already spread to
esophageal cancer).Poor submucosal lymphatics.
survival.
Mostly adenocarcinoma
Carcinoma of Stones in 1/3. Uncommon Obstructive , sudden Jaundice TX: Papillary tumors at the
Extrahepatic Bile Males > Females ampulla can be treated by
Duct resection.
Biliary Atresia Congenital SINGLE MOST COMMON Complete obstruction of the lumen
Main cause of neonatal CAUSE OF DEATH FROM of the extrahepatic biliary tree
cholestasis LIVER DISEASE. within the first 3 months of life.
Acute Gallbladder disease Acute enzymatic ABD pain, N/V TX: Rest. Electrolytes. NG tube.
Pancreatitis Alcoholism necrosis and DIC, shock, ARDS No surgery. Prophylactically
Hyper Triglycidemia inflammation of the Soap formation (Enzymatic fat treat necrosis with Abs.
Obstruction from parasites pancreas necrosis) grossly. Ca++ on pancreas.
Acute ischemia due to Grey-Turner sign bruising of the Auto-immune pancreatitis
obstruction & embolization Release of pancreatic flanks treated successfully by
Drugs (Thiazides, enzymes Fat necrosis Cullens sign bruising around the prednisolone.
mercaptopurine) Fibrosis 2 infection umbilicus
Third space losses. DX: amylase (sensitive, not
Hereditary Pancreatitis: CFTR 85-90% have interstitial Hypocalcemia, hyperglycemia specific), lipase (more
gene Cant spit out enzymes. pancreatitis mild. More severe: specific) WBC count, AST,
PRSS1 gene, SPINK1 gene. 5% mortality severe. Encephalopathy, hypoxemia, ALT, Alk. phos, total bilirubin,
tachycardia, oliguria, azotemia. CRP, IgG4, KUB, Abd US,
Autoimmune pancreatitis: Lots of fluid and necrosis is BAD endoscopic US, CT, ERCP,
High titers of IGg4 Infection common in dead tissue. MRCP
Disorders of the Pancreas
Name Causes /What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Chronic Irreversible damage. Inflammation, fibrosis, Abd pain, steatorrhea when lost DX: CT, ERCP, EUS, Tube tests.
Pancreatitis Alcohol, tropical, genetic, eventual destruction of 95% pancreatic parenchyma,
metabolic, obstructive, auto- exocrine and endocrine weight loss, DM CT can show calcifications in
immune. tissue. the pancreas.
Pancreas divisum When Alcohol pancreas TX: Manage pain CCK via
the duct of Wirsung is only blood flow, oxidative exogenous enzymes. No
draining the ventral pancreas stress, activates alcohol, pseudocyst
and the Duct of Santorini is pancreatic stellate cells. drainage, celiac plexus
draining the dorsal pancreas. blocks, duct decompression.
(Usually these ducts fuse).
Pancreatic enzyme
replacement.
Adenocarcinoma Smoking, drinking 5th most common tumor. Trousseaus Syndrome Migratory TX: Whipple procedure (15%
of the pancreas Many present late, so thrombophlebitis. Cancer associated are candidates)
prognosis sucks. with hypercoagulability.
Obstructive jaundice, PAIN.
Serous Similar to what is seen in 5-15% neoplastic.
cystadenoma of ovary Women > Men
pancreas Benign
Mucinous cystic Can be benign, borderline, Women ONLY (pretty Must be removed to determine
neoplasm of or malignant. much) malignancy.
pancreas
Intraductal Can be borderline or Men > Women
papillary malignant, but tend to be
mucinous low-grade.
neoplasm of
pancreas
Solid- Large solid & cystic areas. Young women
pseudopapillary Low-grade
tumor of
pancreas
Zollinger-Ellison Tumor of G-cells. Gastrin overproduction. May be part of MEN syndromes.
Syndrome 50% malignant
Insulinoma 10% Cancer
Disorders of the Stomach
Typically, the stomach should have no GALT tissue.
Name Causes /What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Heterotopia Congenital
Pancreatic tissue in pylorus
Pyloric stenosis Familial, multifactorial Male > Female Projectile vomiting ~ 5 days 1 DX: Firm, olive in the RUQ.
pattern month after birth. Non-bilious Best palpated after the kid
Turners vomiting (not green) pukes. UGI shows string
Trisomy 18 Emesis electrolyte symptoms sign, US
Acute Gastritis Non-infectious usually. Aspirin and Indomethacin Mucosal insult results in damage of
NSAIDs, EthOH, smoking, are some of the worst. increasing severity.
drugs, uremia, severe stress Acute Ulcers
(intubation, radiation),
ischemia, shock, trauma
(burns, surgery).
Acute Ulcers Stress Bleeds from shallow injuries.
- Burns ~ Curlings Ulcer
- Brain injury ~
Cushings ulcer
NSAIDs, NG tubes and stuff
Chronic Gastritis Chronic inflammation H. pylori is well adapted to Atrophy and metaplasia could be TX: Antibiotics for H. pylori
lymphocytes the stomach flagella, present. DX: Detect H. pylori via Urea
Helicobacter pylori 90% urease and blood group O G-cell hyperplasia breath test, stool exam for HP
chronic gastritis binding. Dysplasia ag. Dont use serum-Ab
Could be auto-immune Active-Chronic gastritis (PMNs in studies (it will only show
Anti-parietal cells. Predisposes to gastric glands) exposure, not presence). BX.
lymphomas of the
stomach
Peptic Ulcer H. pylori almost always Long term invasion of H. Locations of ulcers: First portion of Morphology: Clean and round,
Disease present. pylori leads to ulcers. H. duodenum, Antrum, GE junction, punched out appearance.
Smoking, NSAIDs, steroids, pylori is not in the ulcer. It gastrojejunostomy site, ZE, Meckels smooth borders, flat margins,
impaired emptying, alcohol, is an asymptomatic usually on lesser curvature usually single.
personality, malignancy, viral infection. TX: Daily PPI, stop smoking,
infections, ZE syndrome Pain, bleeding, scarring/stenosis no ASA/NSAIDs, surgery.
Neutralize acid/pain &
healing, block acid
secretion/pain & healing,
repair mucosal
barrier/healing, eradicate H.
pylori.(From Bockman)
Disorders of the Stomach
Name Causes /What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Bezoars Hair ball.
Menetriers Hypertrophic/Hyperplastic Could lead to lymphomas Hypochlorhydria / achlorhydria,
Disease gastropathy of stomach. hypoproteinemia
Large, swollen rugae with lack of
Cause unknown. Very benign condition antral involvement.
Polyps Hyperplastic and Fundic gland polyps Adenomatous polyps have
inflammatory types are show sporadically. malignant potential
associated with chronic
gastritis
Carcinoma of the An Adenocarcinoma Prognosis: DEPENDS ON Usually in pylorus/antrum region
stomach H. pylori?, environment, diet DEPTH OF INVASION. Lesser curvature
(smoked meat) Krukenberg tumor: met to Intestinal type because they exhibit
ovaries intestinal glands.
In US, rates have dropped by Virchows node: Linitis plastica = Leather bottle
85% since 1940s. supraclavicular LN appearance. Signet ring under
Sister Mary Joseph LM.
Nodule: subQ
periumbilical metastasis.
Gastric
Lymphoma
MALT Lymphoma Low-grade B cell lymphoma Non-specific symptoms DX: EGD may be normal
H. pylori infection . mass.
TX: Remove H. pylori.
Celiac Sprue aka Auto-immune disease Damage of intestinal Can appear at birth or later. DX: Anti-endomysial Ab,
Nontropical Intolerance to gluten mucosa and causes Diarrhea, weight loss anti-gliadin and Serum
sprue Strong assoc. with HLA malabsorption. Rare in transglutaminase Ab. Total
DQw2 and B8 Chinese, Japanese, 2x T-cell lymphoma (inappropriate IgA! Confirm with bx.
? Adenovirus type 12? African. T-cell response) Removing gluten improves
Assoc. with: Iron symptoms.
deficiency, LM: Diffuse enteritis, worse in TX: Gluten-free diet
osteoporosis, other duodenum, volous atrophy but
autoimmunities. thickness is the same, lymphocytes,
eosinophils, mast cells.
Gastroparesis Often in DM where nerve Lack of stomach Often associated with GERD.
function is lost in the emptying. (Stomach wont empty, backs up,
stomach. GERD)
Chemo/radiation can
damage nerves
Dysphagia: Sticking sensation. Odynophagia: Painful swallowing. Aphagia: Complete obstruction. Heartburn: Usually due to reflux. Aerophagia: Swallowing of
air. Globus sensation: Lump in the throat.
No alarm symptoms? Treat with PPI for 4 weeks, then f/u. No improvement
EndoscopyAlarm symptoms present? Endoscopy
Adenoma Neoplasm of hepatocytes Young women on oral Usually multiples TX: Stop taking BCPs.
contraceptives
Benign
Malignant Tumors Hepatoblastoma Young 0.5-2% of all cancers in US, Hepatocellular carcinoma Hepatocellular carcinoma
children but up to 20% of cancers in
Angiosarcoma assoc. with areas with endemic HBV
vinyl chloride, arsenic, (China)
Thorotrast
1 carcinoma of liver METASTATIC IS MOST
Hepatocelluar carcinoma and COMMON LIVER CANCER.
cholangiocarcinoma Spotted, random, lots of
times from stomach,
colon, breast, lung
Hepatocellular Cirrhosis HBV, HCV Most are a rapidly Gross: Paler than surrounding liver, Fibrolammelar variant Seen
carcinomas Aflatoxins enlarging mass in well-differentiated to highly in young adults with no assoc.
background of cirrhosis anaplastic. with HBV or cirrhosis risk
No bile ducts, no sinusoids factors. Benign, low-grade.
Pathology of Liver cont
Name Causes / What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Hepatic Drug toxicity after Bone Tender hepatomegaly
complications of Marrow transplantation effects Hyperbilirubinemia
Organ/BM the liver. Centrilobular necrosis /
transplantation inflammation.
May get a veno-occulsive process
(fibrosis around veins. GvH rxn?)
Graft-versus host Liver can be attacked by both Acute 10-50 days after Liver transplants are reasonably BM transplants are worse and
Disease GvH and HvG. Chronic >100d. well-tolerated b/c liver contains lots can cause hepatitis/necrosis
of lymphocytes, establishing a Chronic = Portal
chimerism in the recipient. inflammation and BD
destruction.
Pathology of the Intestines
Intestinal Hernias Most common is inguinal Intestinal obstruction.
hernia.
Whipple disease Tropheryma whippelii White males Malabsorption, diarrhea, big LNs DX: PAS+ macrophages,
Villi LOADED with bacteria small intestine, CNS, joints
TX: Abs (TMP)
Dysentary Low volume, painful bloody
diarrhea.
Shigella
Infectious Viral: Rotavirus (6-25 months) Norwalk from cruise ships.
Enterocolitis Norwalk virus (adults)
Adenovirus (2nd most common
in kids)
Bacterial: Preformed toxin
from Staph
Toxigenic organism (e.g. E.
coli)
Enteroinvasive organism (e.g.
Shigella).
Shigella Bacteria Distal colon, acute mucosal
Enteroinvasive inflammation and exudates
Bloody diarrhea
Pathology of the Intestines
Name Causes / What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Campylobacter Bacteria Villus blunting, superficial ulcers,
jejuni exudates.
Bloody diarrhea
Yersinia Bacteria Can resemble appendicitis Effects ileum, appendix, colon,
Entercolitica mucosal hemorrhage and ulcers
Big LNs with necrotizing
granulomas
Salmonella Effects ileum and colon.
Blunted villi, congestion, linear
ulcers
Vibrio cholera Cholera toxin Activates Cl- Small intestine
(CFTR) channel. Cl- leaves. Na+ in tact mucosa
leaves. H2O leaves.
Clostridium Normal flora bacteria Congestion, some epithelial
perfringens damage
Parasitic Ascaris lumbricoides: Lives in the intestine, larvae penetrate the mucosa and migrates to liver and lung Eggs in the intestine.
Enterocolitis Strongyloides: In ground soil, penetrate intact skin, migrates through the lungs and resides in the intestine
Nacator Duodenale and Ancylostoma duodenale: Penetrate skin, lungs & intestine, attach to mucosa & sucks blood (hookworm)
Enterobius vermicularis: Fecal oral, migrate to anus at night and deposit eggs.
Trichuris Trichiura: Whipworms, does not penetrate mucosa, some may cause bloody diarrhea and rectal prolapsed
Schistosomiasis: Snails.
Intestinal tapeworms: Diphyllobothrium latum, Taenia solium, Hymenolepsis nana. Live in intestine and suck blood.
Entamoeba histolytica: Flask shaped ulcer, liver abscess
Giardia Lamlia: Malabsorption, diarrhea. Drink camping water.
Cryptosporidium: Effects AIDS patients.
Necrotizing Acute necrotizing inflammation Initiation of oral feeding Abd. distension/discoloration, DX: Pneumotosis
Enterocolitis of the intestines in neonates. releases cytokines Gut bloody stools. intestinalis Air in the
Immaturity of the gut immune colonization Mucosal WALL of the intestine. Left-
system PREME problem. injury Lateral decubitus film
Antibiotic C. difficile from Broad spectrum Pseudomembranous colitis
Associated colitis antibiotics killing everything
else.
Idiopathic Ulcerative colitis to Crohns Too much T-cell activation Chronic, relapsing inflammatory DX: P-ANCA+ in 75% of UC,
Inflammatory disease spectrum. and too little regulation of disorders. but only 11% of those with
Bowel Disease Maybe genetics? Infectious? those T-cells when CD.
Abnormal host responding to bacteria
immunoreactivity?
Pathology of the Intestines
Name Causes / What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Crohns Disease Sharply delineated areas Most common in terminal ileum
involved with skip lesions. (but can be from mouth, down)
Granuloma Involves thickening of entire
Smoking is a risk factor. colon.
Non-caseating granulomas
Fissuring, narrow ulcers with
fistulas can go all the way down
TO THE MUSCLE. DEEP.
Creeping fat.
Cobblestone mucosa
Aphthous ulcers (mouth, colon)
Abd, intestinal pain. Obstructive
symptoms.
Ulcerative Colitis Continuous from the rectum Can lead to cancer ONLY THE MUCOSA IS INVOLVED. It LM: Crypt abscesses and loss
No skip lesions . An (untreated = 20-30x risk) is NOT DEEP (like Crohns is) of goblet cells. (Normal, then
extensive broad based Bloody diarrhea symptoms UC below)
ulceration with pseudopolyps Migratory polyarthritis
that involves ONLY THE Sacroiliitis
COLON. Ankylosing spondylitis
Uveitis, Sclerosing cholangitis
Crypt abscesses (inflammation
only in mucosa) Extensive ulceration may lead to
Toxic megacolon.
Chronic Colitis Idiopathic. Different types Diarrhea, cramping pain
depending on what is observed
Diversion colitis, Microscopic
colitis (Collagenous,
Lymphocytic)
Diverticular Acquired Common. GI bleeding, pain, Fe-deficiency
disease Diverticula fill with fecal anemia
Outpouching of all layers of material and become
the intestine. inflamed.
Duodenal Atresia Complete obliteration of BILIOUS VOMITING (Different from DX: Double Bubble on X-
duodenal lumen. pyloric stenosis) ray Stomach bubble,
Polyhydramnios and duodenal bubble. No air
prematurity are common beyond.
ASSOC WITH TRISOMY 21.
Malrotation/ Normally, Cecum is RLQ BILIOUS VOMITING (Because DX: Contrast study. Will see
Midgut volvulus Malrotation Cecum RUQ obstruction is after the duodenum) misplaced Cecum.
very early. TX: Surgery. Cut Ladds
Ladds bands are present for stuff to bands.
twist around Volvulus results.
VOLVULUS IS LIFE-THREATENING.
Meconium ileus/ Intestinal obstructive variant 15% of bbs with CF. Rectal prolapse can be a DX: Barium enema shows
rectal prolapse of cystic fibrosis. complication. Dried out pebbles of
SOOPAR STICKY BABY POOP. meconium in ileum.
Imperforate anus No butthole. Usually present with a fistula which
can lead to just above/below the
anus or into the vagina in girls.
Diarrhea, Constipation, Malabsorption
MOST COMMON CAUSE IF DIARRHEA IN YOUNG ADULTS = CAMPYLOBACTER JEJUNI
Travelers Diarrhea: Enterotoxigenic E. coli
AIDS patients diarrhea: Cryptosporidia
Name Causes / What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Secretory Cholera, VIPoma Large volume, watery diarrhea
Diarrhea Little response to fasting
Osmotic Diarrhea Lactose intolerance IMPROVES with fasting DX: Increased Solute Gap
CHO malabsorption
Fructose intolerance
Mg++ laxatives
Collagenous aka Microscopic colitis because Predominantly older Chronic, watery diarrhea
Colitis looks normal endoscopically, women No bleeding
but has collagen under mucosa
microscopically.
Pancreatic TX: Pancreatic supplement (killed
Insufficiency by stomach acid, so give with PPI
or make sure its coated).
Constipation Inadequate fiber. DX: <2 stools / week, straining,
Drugs. hard stools. Rome II criteria.
Irritable Bowel A group of functional bowel Women > Men Visceral hypersensitivity DX: Rome and Manning criteria.
Syndrome disorders in which discomfort 15-34 years. Abnormal colonic motility TX: Psychotherapy
or pain is associated with **14% incidence, Abnormal brain-GI tract Associated with Fibromyalgia,
pooping. 77% undiagnosed** interactions chronic fatigue syndrome,
Immune activation depression, anxiety, panic disorder
Severe has constant LOTS of bacterial overgrowth. Rape hx or wartime during
symptoms Refer to mental youth. Higher biomarker based
health specialist Dxs as well as symptom-based Dxs.
- Dismotility of the gut can have bacterial overgrowth and, therefore, diarrhea
- Hydrogen Breath Test: Hoomans dont make H2. Bacteria do. So patient eats sugar, then breaths into a bag to measure H2 to diagnose bacterial
overgrowth.
- Pancreatic Insufficiency: CT scan.
- Questions:
o IgA and Ab tests for celiacs.
o Functional vs. Organic diarrhea
o Epidemiology of celiac
o Epidemiology of IBS in US Who decides to go to the doctor?
o Know method for treating *severe* IBS
NUTRITION: