GI - HUGE Table No Hilight PDF

EMBRYOLOGY OF THE GI SYSTEM 3-14-11
- Buccopharyngeal membrane opens ~ 3rd week

- Cloacal membrane opens ~ 2nd month (9 weeks)
- Foregut: Buccopharyngeal membrane to liver diverticulum. Celiac artery
- Midgut: Liver diverticulum to 2/3 of the way down the transverse colon Superior
mesenteric artery
- Hindgut: 2/3 of the way down the transverse colon to cloacal membrane Inferior
mesenteric artery and superior/middle rectal arteries.
- Dorsal Mesentery: Initially continuous down the entire length of the abdominal gut.
Subdivided into meso-regions (e.g., Mesocolon). Dorsal mesogastrium Greater
omentum.
- Ventral Mesentery: Exists only where liver pulled it from the septum transversum.
o Subdivided into lesser omentum (from lesser curvature) and falciform ligament.
- The left umbilical vein runs in the caudal margin of the falciform ligament (right one
degenerates). (Adult = teres hepatis).
- Bile Duct and Hepatic artery run in the caudal margin of the lesser omentum.
- Duodenum bulbs out to form the Gall bladder and Ventral & Dorsal pancreas.
o Twisting of stomach pulls the ventral pancreas to the dorsal pancreas. They fuse
into the adult pancreas. It is intraperitoneal at first, but the mesentery
degenerates, makes it
secondarily retroperitoneal.
o Sometimes the ventral pancreas can be bilobed and during twisting, it will
wrap around the duodenum (annular pancreas) causing bowel obstruction.
- Stomach first flops to the right, then twists clockwise. Left hand to flop and twist.
Thus, Anterior Lesser curvature. Posterior Greater curvature. Left face (left vagus)
Anterior. Right face Posterior.
- Ventral mesentery flopping creates the lesser sac of the abdominal cavity.
- Liver forms in the septum transversum and is therefore not separated from it by
peritoneal membrane. The continuity is recognized in the adult as the bare area of the liver.
The coronary ligament is the reflection of the peritoneum onto the bottom of the
diaphragm. Liver lymph can thus drain via the diaphragm.
- 6-10 weeks Primitive gut loop Pokes out at the umbilicus because there is no
room in the body 270 total (90 on way out, 180 on way in) counterclockwise rotation
Room is made in the body, so it flops back in.
- Cecum originally in RUQ, but descends RLQ.
- 2 Retroperitoneal Structures
o Duodenum (most) (Jejunum & ileum Intraperitoneal)
o Pancreas
o Cecum and Ascending colon (Appendix Intraperitoneal)
o Descending colon (most until the sigmoid Intraperitoneal)
- Urorectal septum partitions the cloaca into the urogenital portion and the anorectal portion (anal membrane ruptures ~ 9th week)
o Point where endoderm meets ectoderm and ruptures at the anal opening changes from pseudostratified columnar epithelium to stratified
squamous epithelium, respectively.
- Oral cavity is lined by a wet stratified squamous epithelium.
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.
- Families of Gut Regulatory Peptides:

o CCK Family: Gastrin, Cholecystokinin, Motilin, Ghrelin
o Secretin Family: Secretin, Glucagon, GIP, VIP, GLP-1, GLP-2,
oxyntomodulin.
o PP Family: PP, PYY, NPY
- Glucose stimulates release of GLP-1 which then stimulates release of Insulin. Glucose + GLP-1 enhances insulin secretion more than if it was just glucose
alone.
- Parasympathetic control is through the Vagus Nerve.
o Vagus nerve is 90% afferent (Transfer from GI tract to brain).
o Cranial preganglionics (Ach, Vagus nerve) efferents go to the entire system all the way through the transverse colon.
o Sacro-pelvic (Pelvic nerve) preganglionics efferents go to the descending colon on down.
o Postganglionics (Ach) are short and on the organ.
- Sympathetic control:
o Preganglionics (Ach) go from Thoraco-lumbar region to the prevertebral ganglia
Celiac
Superior Mesenteric
Inferior mesenteric
o Postganglionics (NE) then go to their respective gut.
- Enteric Nervous System.
o Composed of myenteric and submucous nerve plexuses within the wall of the tract. Again, Substance P, Ach are STIMULATORY. VIP, NO are
INHIBITORY.
OROPHARYNX AND ESOPHAGUS PHYSIOLOGY 3-14-11
- 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
STOMACH PHYSIOLOGY 3-15-11
- 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)
EXOCRINE PANCREAS AND BILIARY SYSTEM PHYSIOLOGY 3-16-11
- 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
- Bile digests and helps absorption of lipids.

- Bile is composed of bile acids, phospholipid, cholesterol, bilirubin
- In the gallbladder, bile is more concentrated than when it comes directly from the liver
cells.
o Concentration occurs through Na+/K+ ATPase. Na+ is pumped out of cells lining
gallbladder, water follows into the capillaries.
- Bile is actively transported into canaliculus.
- Bile salts are made from cholesterol in the liver. They are amphipathic and form
aggregates called Micelles which provide a detergent action for emulsification (stabilize
small fat droplets so they dont bunch together). Regulated via inhibiting the enzyme
that creates them. (Cholesterol 7-hydroxylase)
o 1 - Cholate, Chenodeoxycholate
o 2 - Deoxycholate, Lithocholate formed by bacterial dehydroxylation
o Conjugated To glycine or taurine in liver. All are ionized and exist mainly as Na+ salts.
Conjugated bile acids are recycled through the liver to be used again (95% efficient). They are resorbed into the ileum via a BA-/Na+
apical cotransporter, then pushed into the blood via a BA-/Anion exchanger.
- Bilirubin comes from RBCs hemoglobin (Spleen and bone marrow). It is a waste product that binds to albumin, goes to the liver, then is conjugated with
glucouronic acid. Bilirubin glucuronides are then excreted by the kidney as well as the feces (mostly)
DIGESTION AND ABSORPTION PHYSIOLOGY 3-17-11
- Digestion: Process by which larger ingested

molecules are broken down into smaller molecules
that can be absorbed. Occurs in mouth, stomach,
small intestine via enzymes secreted in these areas.
- Absorption: Process by which molecules are
transported into epithelial cells lining the digestive
tract and then enter the blood or lymph perfusing
that region of the tract. Occurs mostly in small
intestine (nutrients, water, electrolytes) and colon
(water and electrolytes).
- Fat digestion products primarily enter
lacteals of the villus whereas other products enter
the capillaries.
- Enterocytes turn over ~ every 5 days.
- Carrier-mediated (facilitated) diffusion has a
rate of transport which is > than diffusion. Saturation
kinetics are observed where a Vmax is reached when
all molecules are saturated. Active transport
observes the same kinetics, but required energy.
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
- 3 sites of protein digestion

o 1. Lumen from pepsins, pancreatic proteases
o 2. Brush border (glycocalyx) of intestines from brush border peptidases Mainly Aminooligopeptidase.
o 3. Cell body from cytoplasmic peptidases.
- 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
- of fats are from TGs in diet.

- Digestion involves emulsification, hydrolysis and micellar
solubilization (as discussed under histology section of
intestinal mucosal functions below), but
- some esterified short chain FAs like in dairy only
require enzymatic hydrolysis alone
- some require only micellar solubilization, such as
Vitamins ADEK, cholesterol, and trace lipids.
- Without bile salts, 70% of fats can still be absorbed in the upper small intestine.
- Without pancreatic lipases, only 30% of fats can be absorbed. This happens because lingual (glands of von Ebner) and gastric (Chief cells) (acid) lipases
are still present.
- In newborn, pancreatic lipase is decreased, but acid lipases and human milk lipases make up for the difference.
- Acid lipases: TG 1 FA + Diglyceride
- Pancreatic lipase:TG 2 FA + 2-monoglyceride
- Pancreatic Phospholipase A2: Hydrolyzes membrane phospholipids
- Pancreatic Carboxyl Esterase: Hydrolyzes variety of lipid esters.
- Lipase could digest fat droplets fine by itself, but the fat droplets would be HUGE. Bile salts break
those fat droplets into smaller pieces, but keep them from being digested. Colipase allows the
small fat droplets to be digested in the presence of bile salts.
- Fats get into cells by diffusion of some kind. It is not active transport.
- After chylomicrons exit, they enter lymph
lacteals rather than capillaries. They bypass the liver
and enter systemic circulation via thoracic duct.
- Fat soluble vitamins follow absorption of fat.
ADEK.
Water Soluble Vitamins
- Absorbed through variety of mechanisms.

- B12 absorption:
o Salivary haptocorrin from saliva binds
immediately to B12
o Intrinsic factor made by parietal cells
follows this complex into the small intestine.
o Intrinsic factor binds to B12 in the small
intestine and haptocorrin is kicked off by proteases.
o IF + B12 is absorbed in terminal ileum
then stored in the liver.
Water and Electrolytes
- Osmolality of a meal becomes isotonic with passage through the duodenum

movement of water via osmosis.
- Most H2O absorption occurs in jejunum & duodenum.
- Diarrhea: When H2O isnt absorbed as much as it is supposed to be.
- Water absorption depends mostly upon the absorption of Na+.
Calcium
- Absorbed in duodenum at a greater rate than for other divalent cations.

- Ca++ serum PTH 1,25 (OH)2 Cholecaciferol calbindin-D proteins
and Ca++ ATPase in enterocytes
Iron
- Absorption increases with need (hemorrhage, growth, pregnancy)

- Carrier-mediated transporters on brush border for Fe2+ and Heme. Amount absorbed is regulated by enterocyte ferritin levels. Fe2+ bound to ferritin
cannot be used by the body.
Note water and Cl- transports above. Also note Cholera toxin, how it
stimulates Cl- to be transferred, therefore Na+, therefore H2O into the lumen.
Elecrtrolyte and Water transport in the Colon
- 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
- Cellulose, hemicelluloses, pectins, mucilages cannot be hydrolyzed by human enzymes.

- It can be metabolized by colonic bacteria to short-chain FAs which are passively absorbed.
- Increases stool weight, frequency (increase in luminal osmolarity), and decreases water
absorption.
Gas Accumulation in GI Tract
- Swallowed air
- H+ + HCO3 CO2
- Bacterial fermentation
INTESTINAL MOTILITY 3-18-11
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.
COLONIC MOVEMENT PATTERNS
- Colonic response to a meal is initiated by signals from the stomach and

intestine.
Developmental Disorders
Name Causes Pathogenesis Clinical Diagnosis/Treatment/Other
Hirschsprungs Lack of Neural crest doesnt migrate correctly into the Rectum always DX: Baby fails to pass poo
Disease aka parasympathetic hindgut, and so there is no parasympathetic involved. within 24 hrs. XR shows
Congenital innervation of innervation. Thus, sympathetic overrides and Megacolon. megacolon.
Aganglionic hindgut. makes it squeeze shut. Food backs up and TX: Colostomy
Megacolon creates a megacolon.
Abnormal or Absent Biggest challenge is
Anal sphincter reconstruction of the
opening. sphincters.
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.
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.
Gastro- aka Cardiac Wet stratified squamous epithelium

Esophageal region transitioning to simple columnar epithelium.
Junction
Mostly mucus secretors Protect
esophagus from gastric acids. (Seen also in
the pyloric region) Can secrete Bicarbonate
to lower the pH.
Stomach Wall Rugae.
(not cardiac Simple columnar epithelium Mostly mucus
region) secreting.
Gastric pits give rise to glands that dip down
into the lamina propria.
Stem cells Renewing epithelial cell layer, at
bottom of pit. .
Glands: (seen mostly after pit)
1. Parietal Cells Acid secreting cells.
2. Chief Cells Pepsinogen and digestive
enzymes made here. Darker pink, deeper than
the parietal cells
3. Mucus Neck Cells Make the mucus. Goblet
cells. Dr. Nichols: They all shoot their wad at
once. Contain mucus granules
4. APUD / Enteroendocrine Cells Produce
hormones, like serotonin, somatostatin, etc.
Small, lighter colored cells wedged up against the
chief cells.
Muscularis 3 layers of 1. Outer layer Strongest at outer and inner
Externa/Propri muscle curvature of stomach.
a of the surrounding 2. Middle, circular layer forms the pyloric
stomach the stomach. sphincter and becomes continuous with the
circular layer of the gut.
3. Inner, longitudinal layer.
GI Histology
Tissue Function/Features LOOK/Other
Basic Liver Inputs: Artery, Portal Vein
Outputs: IVC, Bile
Healthy liver can Basic Unit: Hepatic Lobule Hexagonal with a central vein in the middle and portal
be binucleate or areas surrounding at each vertex. Each portal area has a portal triad (hepatic
some cells can artery, portal vein, bile ductalso see a lymph vessel as well. ) Portal veins and
be tetraploid. hepatic arteries are connected to the central vein/Terminal Hepatic Venule via
sinusoids (capillaries which have holes in them large enough to pass material).
Bile Ducts go in between the sinusoids, and the terminal branches of these give rise
to hepatocytes.
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.
Endocrine Islets of Langerhans. = Glucagon. = Insulin

Pancreas
GI Histology
Tissue Function/Features LOOK/Other
Gallbladder
Intestinal Features:
Mucosa Plicae Circulares / Valves of Kerckring: Gross ridges lining the intestine.
Villi: Lined by simple columnar epithelium (enterocytes) Absorb materials.
Also see goblet cells intermittently Mucous secreters without a brush border.
Lots of Golgi to make mucous.
Duodenum Short, thick plicae
Jejunum Long, thin plicae
Colon No projections. Flat surface.
Stem Cells: Further down in villus, regenerating enterocytes which progressively
migrate up the wall of the villus to the tip. At the tip, they slough off. Some of them
however, will migrate down to form Paneth Cells at the bottom of the gland. They
are located at the base of the gland versus at the neck of the gland as seen in the
stomach.
Paneth Cells: Secrete eosinophilic material used for host defense lysozyme (so
dont confuse them with eosinophils).
Open/Closed Enteroendocrine Cells: Secrete various kinds of hormones into the
underlying connective tissue (not the lumen)Open = surface visible to lumen. Closed =
Focused mostly on the basal end of the cell layer.
Intestinal Glands / Crypts of Lieberkuhn: Paneth cells reside here.
Glycocalyx: Contains the final enzymes needed for digestion all anchored to the cell
membranes. A thin layer resting on top of the microvilli.
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.
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.
Irritation Fibroma Trauma MOST COMMON SOFT TISSUE Benign proliferation of

LESION OF THE ORAL CAVITY. tissue.
Basically a scarring of tissue.

Bite Inflammation Healing
Scar
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.
Peripheral Giant Cell Tons of giant cells in the tissue.

Granuloma (Macros)
Aphthous Ulcers / Idiopathic. Necrosis of the epithelium. Ulcer. TX: Self-limited

Cold Sores / Canker Local T-cell immune NOT DUE TO HERPES. Pain out of proportion to
Sores dysfunction Opposite to herpes!! size of lesion.
Stress. Peripheral red halo.
Assoc. with Celiac, Crohns,
Reiters, HIV, PFAPA, Behcets
Hyperplasia of gums DILANTIN / PHENYTOIN
Seizure drug
Traumatic Ulcer Trauma. Hot pizza, ASA Lateral tongue ulcers in Could look like cancer
sitting on tissue, cotton overweight, middle-aged
rolls, factitial (psychiatric males with sleep apnea
disorder)
Geographic and NORMAL. A large proportion of geographic
Fissured Tongue tongues are fissured.
Glossitis Vit. B deficiency Flat, shiny tongue.
Pernicious anemia
Iron deficiency anemia
Acute Leukemia MONOCYTIC LEUKEMIA = Swollen, bleeding gums.

leukemia most often
assoc. with oral lesions
Primary HSV HSV-1 (genital HSV-2) Physical contact transmission. Mostly seen inside lip.
Primary Heprpetic 1st infection with HSV.
Gingivostomatitis Mostly young children.
Recurrent HSV First sunlight of the Especially seen in lip

season. vermillion (at the border
Cold, trauma, stress, of the skin and lip)
menses
Measles Koplik Spots
Mumps aka Endemic Paramyxovirus Parotitis Prevention: MMR vaccine
parotitis Orchitis
Encephalitis
Erythema Multiform Drug reaction & reaction Minor, major, and Toxic
to viral infections. epidermal necrolysis
Leukoplakia 5% cancer White Patch
Erythroplakia 50% cancer. Red Patch
Actinic (Solar) Sun Tissue degeneration Preneoplastic Malignant
Cheilitis secondary to chronic transformation 6-10%
sunlight exposure. On the lower lip with blurring of
the vermillion border.
Pale to whit ehyperkeratotic
plaques.
Cracking/scaling of lips.
Oral Squamous Cell Smoking, chewing, 50-70yo. AA Males. 50% Floor of mouth, tongue most STOP SMOKING.
Carcinoma EthOH fatal. common. TX: Surgical excision, F/U.
HPV of tonsil (16,18) Lower lip presentation has Non-healing lesion (red or white
good prognosis. Everything or mixed)
else is bad. Outgrowth (exophytic)
Verrucopapillary (more common
smokeless tobacco users)
Cervical lymphadenopathy = oral
cancer until proven otherwise.
Smokeless tobacco Smokeless tobacco Stained teeth.
Keratosis Gingivitis.
White/fissured patches of mucosa
Periapical Abscessed tooth Inflammation causes
Granuloma destruction of part of the
bone.
Periapical / Seen as lucid, cystic area in the gum
Radicular Cyst (actually filled with granulation
tissue, so it isnt a true cyst)
Dentigerous Tooth never erupts True cysts are lined by Cyst seen on Crown of impacted
(Follicular) Cyst epithelium. tooth
Odontogenic Follicle filling up with TX: Remove epithelium.
Keratocyst desquamated squamous
cells.
Ameloblastoma Mostly benign, but Asymptomatic
aggressive. Seen on posterior mandible.
Recurrence common Resembles enamel organ.
Odontoma Malformed tooth. Mostly benign.
Hamartoma (Right tissue,
wrong amount)
Neck and Salivary Gland Disorders
Mucocele Severance of minor Mucus released into Squishy, usually.
salivary duct surrounding connective
tissue instead of out of pore
where it is meant to go.
Salivary Gland Mostly in the parotid.
Neoplasms (General Most benign in the parotid. (Rule of 80s 80% are benign, and 80% of those are Pleomorphic adenomas)
characteristics) Most malignant elsewhere. (Submandibular = 40%, Sublingual = 90%, Minor salivary glands = 50%)
Smaller gland = More likely to be malignant cancer.
Women > Men, (except Warthins) usually 40-60yo.
Palate is most common site for minor salivary gland neoplasms.
Pleomorphic Radiation exposure. Malignant type is rare (only Mixed tumor Cartilage/bone
Adenoma 2-10%) Ductal and myoepithelial cells.
MOST COMMON SALIVARY 60% of parotid tumors
GLAND TUMOR
Warthins Tumor aka Heterotopic SG tissue Mostly men. ONLY in the parotid.
Papillary with parotid lymph node. Doughy, cystic mass.
Cystadenoma Tobacco smoking (The Benign
Lymphomatosum only salivary gland
tumor linked to
smoking)
Mucoepidermoid Radiation exposure. Most common malignant Mixed tumor Adenoid and Could
Carcinoma salivary gland tumor. But squamous. Squamous component mimic a
mostly low-grade, so is the malignant part. mucocele.
prognosis is good. Mostly in parotid.
Adenoid Cystic Most common malignant Can recur, so has a good short term Cribriform or Swiss-cheese
Carcinoma tumor in non-parotid glands. survival, but POOR long-term. pattern.
Tends to grow around nerves.
Sialolithiasis Stone in salivary gland Leads to inflammation and
duct atrophy of SG b/c of clog.
Sjogrens Auto-immune Destruction of glandular Dry mouth.
structures leaving only
ducts.
Thyroglossal Tract When thyroglossal duct Foramen Cecum Thyroid ALWAYS MIDLINE
(Duct) Cyst doesnt all regress. gland descent.
Branchial Cleft Cyst Brachial cleft didnt Teens-20s ALWAYS LATERAL
resolve.
Laryngeal Tobacco + alcohol
Carcinoma
Disorders of the Esophagus
Esophagus has a single longitudinal muscular mucosa. (None circular)
Name Causes /What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Esophageal Congenital. Frequently assoc. Aspiration, suffocation, TX: Surgery
Atresia with polyhydramnios / pneumonia, severe fluid and DX: Oral gastric tube stops
premature labor. electrolyte imbalances. in mid-throax. Air in
Esophageal Congenital. More common than atresia, Excessive drooling or stomach indicates distal
Fistula with most common being B choking on first feeding. TEF. More difficult to dx H-
above:atresia w/ distal fistula type because baby can eat.
Hernias Protrusions of stomach into
thoracic cavity.
2 Types: Sliding and
paraesophageal
Diverticuli 2 Types: True (all layers Subtypes: Zencker
outpouching) and False (mucosa Zencker Diverticulum =
and submucosal) Pharyngoesophageal. Could
be assoc. with TB.
Mid-portion
Distal
Mallory-Weiss Esophageal lacerations seen in Excessive vomiting. Massive

Syndrome alcoholics bleeding.
Webs Squamous mucosal protrusions in
upper esophagus.
Rings Concentric proliferation of mucosa
and submucosal with
hypertrophied muscle in the distal
parts.
Achalasia Failure to relax the Lower Lack of relaxation Progressive weight loss, chest DX: Barium esophagography
Esophageal Sphincter. Dilation of esophagus pain shows birds beak.
1 - Congenital problem of neurons Degeneration of neurons in Triad: endoscopy (R/O
2 - Scarring, etc to esophagus myenteric plexus 1. Incomplete LES relaxation pseudoachalasia)
2. Increased LES tone TX: Pneumatic dilation,
3. Aperistalsis of esophagus surgical myotomy, BOTOX.
Esophageal EthOH cirrhosis, chronic Portal blood flow is diverted Massive hemorrhage, GI
Varices hepatitis, Wilsons through stomach and bleeding (Black, tarry)
Dilated submucosal vessels esophageal vv. into azygos v.
secondary to portal hypertension 40% of people die of
creating collateral bypass channels bleeding at the first
between portal and caval systems. episode.
Esophagitis Infectious (In those who are
immunosuppressed. bacteria,
fungus, HSV, CMV), EthOH,
chemotherapy, uremia (causes
gastroenteritis), drugs
(Tetracycline when they dont
get washed all the way down)
Eosinophilic Dense eosinophilic mucosal Young males Dysphagia from strictures LM: 15-25 eosinophils per
Esophagitis infiltrate Chest pain HPF.
Longitidinal furrows or TX: Fluticasone inhaler
circular ridges
Reflux Chronic Reflux esophagitis. Reflux path: Acid gets up into Stricture, bleeding, ulcers LM: Eosinophilic
Esophagitis / Reflux of gastric acids and bile. esophagus and eats the tissue. Nocturnal cough inflammation, basal cell
Gastro- (Bile is basic pH 8, and VERY Body repairs Metaplasia Frequent sore throat hyperplasia, elongation of
esophageal damaging) over years Metaplasia is Hoarseness, laryngitis papillae with congestion.
Reflux Disease Alcohol, tobacco, obesity, CNS acid-resistant. Exacerbation of asthma TX: Sleeping more upright,
depressants, pregnancy, poor Globus sensation PPI, H2 blockers, surgery.
esophageal clearance, hiatal DX: Endoscopy is insensitive
hernia, delayed gastric emptying.
Barretts Intestinal metaplasia above GE BE will develop in 6-12% pts Will see goblet DX: CDX2 (not normally
Esophagus junction with GERD. 3-5% will progress cells under LM seen in esophagus and
to adenocarcinoma. bx (intestinal stomach)
Low grade dysplasia High type) TX: Neither anti-reflux meds
grade dysplasia Indefinite or surgery will reverse the
dysplasia epithelial cell changes.
Surveillance via endoscopy.
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.
Leiomyomas Benign, most common tumor in

esophagus
Squamous Smoking, alcohol, possibly Most common esophageal Pain, difficulty swallowing, TX: Surgery
carcinoma of genetic, B12 deficiency. cancer WORLDWIDE. Will weight loss, hematemesis,
esophagus usually be high-stage vomiting, chest pain.
because there is no serosa in Most already spread to
esophagus to protect, so it submucosal lymphatics.
SPREADS FAST.
Dysphagia Transfer (oropharyngeal) type: Could be an intrinsic Mechanical obstruction
Difficulty transferring food from narrowing or an extrinsic Primarily problem with solid
the mouth to the esophagus. compression problem swallowing, progressive in
Cough, choking, usually nature, weight loss.
neuromuscular (Parkinsons, Motility disorders
ALS, MS) Primarily problem with solids
Transport (esophageal) type: AND liquids, intermittent,
Trouble transporting food from associated with chest pain
the upper esophagus to the and esophageal diverticula.
stomach food sticks.
Odynophagia Ulceration of the esophagus, Pill-induced: TCN, NSAIDs,
trauma, or infectious esophagitis Bisphosphonates, KCl,
(candida, HSV, CMV) Quinidine, Ferrous sulfate
Diffuse Simultaneous non-peristaltic Low amplitude DX: Corkscrew esophagus
Esophageal contractions of the esophagus. contractions. Poor bolus in barium study. Esophageal
Spasm transit. manometry (pressure)
Nutcracker Increased pressures during High amplitude contractions,
Esophagus peristalsis. chest pain.
Scleroderma CREST syndrome (E = Esophageal Poor distal peristalsis.
dysfunction) Decreased LES tone.
Severe reflux.
Heartburn Retrosternal burning. Must discern between Cardiac
Regurgitation. and Non-cardiac chest pain.
Exclude cardiac before
esophageal causes in elderly
patients.
Hiatal Hernia Upper portion of stomach slides Alters angle of His and loss of Symptoms arise with giant TX: Reflux surgery.
above the diaphragm. diaphragmatic component of hernia.
Obesity, age LES.
Dyspepsia Epigastric fullness, postprandial 2/3 are functional diseases: Upset stomach. DX: Rule out H. pylori, PPI to
pain, belching, bloating, nausea, Ulcer-like, dysmotility-like. r/o gastritis, endoscopy for
food intolerance. alarm symptoms.
Happy St. Pattys Day!
Gallstones Obesity ( cholesterol 10% of the population Majority are asymptomatic, Smalls Triangle: 3 sides =
aka with bile) 2 Types: found incidentally. [cholesterol], [phospholipids],
Cholelithiasis Diabetics 1. Cholesterol Stone [bile salts]. cholesterol,
Cirrhosis (Pigment - Most common in US. Yellow, round, Symptomatic: Wedged into bile salts, phospholipids
gallstones) smooth/mulberry/ facetted. the neck of the gallbladder (lecithin) = Soluble material.
Hemolytic diseases Lithogenic bile has high cholesterol. (Biliary colic) or in the bile Anything else can lead to
(Pigment stones) When in the gallbladder, it is in stasis, duct. stones.
Age ( sensitivity to cholesterol crystals form in a process called
CCK) nucleation eventual stone. Neck of gallbladder DX: XR (only 10% gallstones
Pima Indians Biliary colic: Some of the are Ca++), CT (again, only 10%
(Hereditary) 2. Pigment Stone worst pain you can get. RUQ are Ca++). Most accurate and
Crohns (IBD that Normal Inflammation: acute gold standard= US.
bile salt reabsorption Hgb in RBC Heme Biliverdin cholecystitis / edema of the
cholesterol stones) Bilirubin + albumin Released from gallbladder Pain, fever, TX:
Typhoid Fever albumin in liver + glucuronyl transferase N/V; + Murphys sign; Asymptomatic No tx,
(Salmonella) Conjugated bilirubin + glucuronidase empyema from normal flora unless immunocompromised,
Unconjugated bilirubin Excreted in migrating to it; gangrene of b/c they dont handle gall
Cholesterolois feces. gallbladder From septic stone complications well.
cholesterol deposits on Pathological thrombi forming.
mucosa of gallbladder. Black stones: Chronic Excess hemolysis Perforation: gall stone ileus Symptomatic Bile acids,
excess unconjugated bilirubin is insoluble Gall bladder is inflamed contact solvents given through
and forms black stones in the gall bladder. and fuses to duodenum, stone catheter, mechanical
ruptures through wall, passes extraction (ERCP),
Brown stones: Conjugated bilirubin enters through bowel to the terminal cholecystostomy,
bile duct FB is already present in gall ileum, Mirizzi Syndrome choledochoscopy,
bladder causing chronic cholangitis (A. Chronic inflammation. fragmentation. (All of these
lumbricoides, liver flukes, other stones) E. Carcinoma of gallbladder: only temporary b/c take away
coli (normal flora) in gall bladder creates always assoc. with stones. symptoms, not source). Gold
unconjugated bilirubin by infection forming standard cholecystectomy.
around FB Ca++ bilirubinate Brown Bile Duct
stones in the bile ducts (Choledocholithiasis) ERCP of stones in common
Jaundice: From obstruction bile duct to remove them.
Bile made out of: Cholesterol, Ascending Cholangitis: Pain,
phospholipids, Bile salts, Bilirubin, Ca++, fever, jaundice.
Na+, Water Acute Pancreatitis: Stone
pushed through Sphincter of
Oddi Injures it Reflux of
enzymes back into pancreas.
Happy St. Pattys Day!
Gall bladder has no muscularis mucosae
Spiral valves of Heister are in the neck of the gallbladder Stones commonly stuck here.
Ducts of Luschka
Rokitansky-Aschoff Sinuses
Chronic Stones almost always present. Porcelain (calcium), hydrops Histology: Rokitansky-Aschoff
Cholecystitis (mucus)
TX: Cholecystectomy
Complications: As discussed above
with stones Perforation, gall stone
ileus, infection, gangrene
Gallbladder Associated with stones in the RARE
tumors US, less so where GB infections Terrible prognosis
(parasites schistosomes,
liver flukes) are common.
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
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.
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
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.
Alarm Symptoms: Odynophagia, Weight loss, recurrent vomiting, intestinal

bleeding, jaundice, palpable mass or lymphadenopathy, Fam hx of GI
malignancy. MaL VOW BJ
No alarm symptoms? Treat with PPI for 4 weeks, then f/u. No improvement
EndoscopyAlarm symptoms present? Endoscopy
In hospital, administer NSAIDs with either Prostaglandin E analogue

(misoprostol) or PPI.
RANSONS CRITERIA To eval. severity of pancreatitis

More of these you have, the more your mortality goes up.
DRUGS USED IN GI DISORDERS (Notes to accompany drugs)
- H. pylori damages/colonizes the cytoprotection

layer and exposes the stomach cells to the low pH.
- cAMP is the most efficacious method of activating
the proton pump. Thus, blockage of the cAMP
pathway is the most efficacious way to block
acid.
- H2 is the most important acid regulating receptor.
- ECL cell = Enterochromaffin-like cell.
- Note how PGs not only block acid, but promote
secretion of mucous and HCO3.
Pathology of the Liver
CHF = Less blood to the outer lobule = hepatocyte damage = AST/ALT
Bile duct damage = alk. phos.
5 Patterns of Hepatic Injury:
1. Degeneration and intracellular accumulation (fatty-change steatosis)
2. Necrosis and Apoptosis tends to be zonal (i.e., Hepatitis, drug rxns)
3. Inflammation hepatitis
4. Regeneration
5. Fibrosis / scarring cirrhosis in the liver
Name Causes / What is it Pathogenesis Clinical Diagnosis/Treatment/Other
Jaundice 1. Excessive production of Normal bilirubin = 0.3-1.2 Creases of hand can be Sometimes have to rely on family
bilirubin Jaundice = 2.0-2.5 yellow. members whether or not the
2. Reduced hepatocellular person is yellow
uptake Normal Yellow/green. But mostly
3. Impaired conjugation Heme Biliverdin yellow.
4. hepatocellular excretion Bilirubin/Albumin complex
5. Impaired bile flow Conjugated bilirubin in
hepatocyte Conj. bilirubin
in bile Metabolized in
colon BA reabsorbed,
waste excreted.
Hereditary Crigler-Najjar syndrome Gilber syndrome AD, Dubin-Johnson syndrome Rotor Syndrome AR, defects in
Hyperbilirubinemia (death sentence) Genetic expression UGT, 6% of AR, impaired biliary hepatocyte uptake and excretion
lack of bilirubin UGT (enzyme population excretion of bilirubin
responsible for conjugating glucouronides (already
bilirubin) conjugated)
Cholestasis Biliary obstruction Cant Could be intrahepatic or Jaundice
get bile out of the liver. extrahepatic. Pruritis (from BA)
Skin xanthomas
Bile pigment is within the Alk. Phos.
hepatic parenchyma. Intestinal malabsorption +
Dilated bile canaliculi / deficiencies of vit. ADK (Also
bile lakes with distension E, but it is less-so)
of upstream bile ducts
leads to proliferation of
ducts, inflammation and
portal tract fibrosis.
Pathology of Liver cont
Hepatic Failure Loss of 80-90% of hepatic Jaundice, Hypoalbuminemia Reyes Syndrome Hepatic
activity. Edema (because all albumin in body is dysfunction without overt
Massive hepatic necrosis made in liver), hyperammonemia necrosis. Pediatric disease.
(because we cant metabolize them),
Could be viral hepatitis, fetor hepaticus (musty sweet &
drugs, chemicals, sour smell), Impaired estrogen
mushroom poisoning, but metabolism (palmar erythema, spider
most commonly hepatitis angiomas, gynecomastia),
or alcohol Coagulopathy (2, 7, 9, 10 factors
made in liver), Hepatic
encephalopathy Consciousness
variable, asterixis (liver flap)
Cirrhosis Scarring/fibrosis of the Progressive fibrosis Hepatic Bridging fibrous septa from portal
liver. stellate cells (Ito cell) is the area to portal area and/or central vein
Disruption of the source of collagen. They
architecture of the entire normally store vit. A Regenerating parenchymal nodules
liver with vascular transform into myofibroblasts. that dont hook up to architecture
architecture reorganized. Chronic inflammation produces correctly. .
cytokines (TNF, TGF). Cytokine
Usually caused by alcohol production is stimulated by Silent for a long time.
in US, but also viral endogenous cells. ECM Anorexia, weight loss Symptoms
hepatitis and biliary disrupted. Stellate cells of overt hepatic failure.
disease. 10-15% are stimulated. PORTAL HYPERTENSION.
unknown. DEVELOPMENT OF
HEPATOCELLUAR CARCINOMA.
Portal Increased resistance to Backup Outlets = Esophagus, Ascites Excess fluid in peritoneal TX: Porto-systemic shunts
Hypertension portal flow at the level of Umbilicus, spleen, cavity
the sinusoids and hemorrhoidal/rectal veins. GI bleeding and intestinal fluid leakage
compression of central Renal retention of Na+ due to 2
veins by perivenular hyperaldosteronism
fibrosis Splenomegaly
Hepatitis A virus Highly infectious. Fecal-oral spread IgM Ab against HAV present at time If they only have IgG, its
(HAV) SSRNA picornavirus Low mortality rate. of symptoms. IgG Ab persist for years probably not HepA (though
No chronic form. providing protective immunity. theyve had it in the past)
Will NOT turn fulminant. Anorexia, jaundice, malaise TX: Self-limited
Hepatitis B Acute hepatitis - 4-26 DX: HbsAg screen. Appears
(serum week incubation in blood before the onset of
hepatitis) symptoms.
DNA virus
Some patients may recover
Nucleocapside core fully, but others may
proteins (HBcAg and develop chronic HepB.
HBeAg)
Envelope Has an integrative phase
glycoprotein viral DNA is incorporated
(HbsAg) into the host genome and
Hepatocytes can not destroyed.
synthesize massive
quantities of this. HBeAg, HBV-DNA and DNA
DNA polymerase pol. signifies active viral rep.
Protein from the X
region (HBX) Anti-HBeAg detectable shortly
necessary for viral after the HBeAg has
replication disappeared is a good sign
The virus has been conquered.
Hepatitis C virus SSRNA Flavivirus High rate (85%) of progression Eventual cirrhosis DX: HCV-RNA is detectable in
IV Drug abuse to chronic hepatitis Course is milder than HBV blood at time of symptoms
Multiple Sex partners AST, ALT
Surgery w/in 6 mos. Can lead to hepatocellular
Needle stick carcinoma
Hepatitis D Virus Delta virus Works in conjunction with HepB
Gives it a more dramatic and
progressive course.
Acute Viral Peak infectivity occurs during LM: Diffuse swelling of
Hepatitis last days of incubation. hepatocytes and portal
Preicteric phase Nonspecific triads, cholestasis, clumps
constitutional symptoms, some of macros, apoptosis
immune complex symptoms (eosinophilic councilman
bodies) Kupffer cell
Arthritic symptoms in hypertrophy, portal tracts
preicteric phase. with WBCs in them, fatty
No jaundice in 50% change in HCV
Chronic Viral Biochem or serologic Persistent AST/ALT LM: Ground-glass cells
Hepatitis evidence of continuing Vasculitis, glomerulonephritis, (HBV), predominantly
disease for 6mo+ cryoglobulinemia lymphoid aggregates in
Interface hepatitis = piecemeal portal tract, FIBROSIS FROM
necrosis. CENTRAL VEIN TO PORTAL
Cirrhosis. AREA (cirrhosis)
Fulminant HBV, HCV (less than 50- Rapid onset of hepatic Small flabby liver (acute yellow
Hepatitis 65%) insufficiency (w/in 2 weeks) atrophy)
Drugs, chemical toxicity
Acetaminophen,
Isoniazid, anti-
depressants, halothane,
amanita phalloides
Autoimmune Unknown etiology (HAV, Autoimmune attack from IFN-, ANA, anti-smooth muscle, anti-
Hepatitis HBV, HCV negative, no CD4, CD8 microsome.
lupus, no scleroderma) Clusters of plasma cells in portal
Usually women areas with interface hepatitis
Alcoholic Liver Ingestion of 8 beers Fatty change shunts normal Fatty change Micro and macro- LM: Mallory bodies (clumps
Disease produces mild reversible substrates away from vesicular lipids. of cytokeratin filaments),
fatty change. Doing this or catabolism and lipid Alcoholic hepatitis Acute hyaline PMNs, Fibrosis around central
more daily risk of severe biosynthesis. sclerosis. (AST > ALT) vein, steatosis = big fat
liver disease Alcoholic cirrhosis (irreversible) vacuoles.
Non-Alcoholic Hepatic steatosis who dont NAFLD leads to NASH Cryptogenic Cirrhosis and
Fatty Liver drink alcohol (<20g Hepatitis
Disease & EthOH/week)
NASHepatitis Obesity, DM, post gastric
banding
1 Excessive accumulation of Fe - 50-60 Micronodular cirrhosis, DM (wipes
Hemochromatosis Homozygous recessive Chr. 6 - 70-80 out islet cells), skin pigmentation
(bronze)
2 Excessive Fe+ due to excess rarely causes severe symptoms.
Hemochromatosis transfusions.
Chronic hemolytic anemia
(thalassemia major)
treatment.
Wilson Disease Accumulation of copper in Cirrhosis
tissues. Neuropsychiatric manifestations
Kayser-Fleischer rings in the iris
-1 Antitrypsin AR Low levels of the protein Panacinar emphysema OR
Deficiency A defect in the migration of the that inhibits proteases that cirrhosis
secretory protein from the ER to are released by PMNs
the golgi Get stuck during inflammation.
PiZZ genetics.
1 Biliary Inflammation of the bile duct Middle-aged women Portal inflammation and
cirrhosis locally. probably autoimmune (80%) scarring/fibrosis
Chronic, progressive cholesttic Non-suppurative, granulomatous
liver disease. destruction of medium-sized
Destruction of the intrahepatic intrahepatic bile ducts.
bile ducts Alk. phos.
Anti-mitochondrial antibodies
2 Biliary Inflammation of the bile duct, yellow-green pigmentation of the
cirrhosis *not* due to the bile duct locally liver
(Obstruction) Hard finely granular appearance of
Cholelithiasis liver.
Malignant neoplasms of Portal fibrosis with distended
biliary tree or pancreas small and large bile ducts.
Strictures from prev. surgery
Primary Seen with IFB Males >Females Onion-skin fibrosis No auto-ab association.
Sclerosing Caused by infections Disappearing bile duct.
Cholangitis Inflammation, fibrosis and Jaundice
segmental constriction of Pruritis
the intrahepatic and
extraheptatic bile ducts.
Other Liver Bacteria: Staph, S. typhi (Typhoid Flukes cause abscesses and fibrosis.
Infections fever) T. palladium
Liver flukes
Schistosomiasis (bile ducts)
Von Meyenburg Bile duct hemartomas Benign. Bile ducts formed Cystic-appearing with little nodules
Complexes wrong. around it. Can be confused with
metastasis.
Polycystic Liver Simple cysts No destruction of the liver as seen in
Disease Can be assoc. with PCKD PCKD to kidneys.
Congenital Not due to usual cirrhosis.
Hepatic Fibrosis
Caroli Disease Larger ducts of the intrahepatic Not clinically relevant.
biliary tree are segmentally
dilated
Echinococcal cysts Echinococcus granulosus
tapeworm.
Hydatid cysts
Amebic abscess of Entamoeba histolytica Invades the mucosa of the Anchovy paste cysts
the liver intestine and causes an
ulcer portal system
Stuck in liver Cyst
Passive Right-heart failure. NUTMEG LIVER
congestion of the Sustained failure Cardiac
liver sclerosis (rare)
Centrilobular necrosis
AST/ ALT
Peliosis hepatis Sinusoidal dilation assoc. with
anabolic steroids
Bartonella henselae in HIV pts.
Hepatic vein Hepatic vein outflow Ascites
thrombosis / obstruction. Hepatomegaly
Budd-Chiari polycythemia vera Abd pain
syndrome post-partum state AST/ ALT
Oral contraceptives Jaundice
Preeclampsia and Pregnancy hypertension Fibrin into space of Disse, HELLP syndrome Acute fatty liver can also occur
Eclapsia leading to periportal Hemolysis in pregnancy.
hepatocytic necrosis. Elevated Liver enzymes
Low Platelets
Focal Nodular A well demarcated nodule Young women Central gray-white stellate scar.
Hyperplasia Very benign
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.
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.
Intestinal Surgery is most common Will be fine so long as

Adhesions cause. twisting doesnt occur.
Intestinal Telescoping of the intestine on Common in kids. In adults, Strawberry jelly stool.
Intussusception itself usually a tumor or polyp
which tugs the rest of the
bowel down when stool
is passing by.
Intestinal Twisting of intestine on itself
Volvulus due to adhesion or other reason.
Ischemic Bowel hernias, adhesions, Infection + Necrosis
Disease intussusception, Volvulus,
arterial thrombosis, arterial
embolism, venous thrombosis
(hypercoagulation, BCPs),
monoclusive ischemia (CHF),
radiation.
Angiodysplasia Tortuous dilations of Significant lower gut hemorrhage
submucosal and mucosal blood
vessels
Hemorrhoids Dilations of anal venous
plexuses.
Heterotopia Ectopic pancreas or stomach in Symptoms may occur if tissue is
small bowel. functional.
Meckel Ectopic gastric/pancreatic tissue Within 2 feet of ileocecal
Diverticulum valve.
Malabsorption Suboptimal processing of food. Can be fat, protein, carbs, Presenting signs/symptoms could
general Pancreatic insufficiency (CF) water, salt. Since digestion be in another system. (Fe++-
characteristics Biliary obstruction starts at mouth Colon, deficiency anemia e.g.)
Bacterial overgrowth (abs) culprit could be anywhere. Steatorrhea
Reduced surface area Diarrhea
Lymphatic obstruction (TB) Abd. pain
Infection Weight loss
Tumor Vit. D, calcium, Vit A, B12, Vit K
Many others deficiencies
Tropical Sprue In the tropics, endemic and Diarrhea, malabsorption
epidemic forms Variable histology, but usually
more diffuse than celiac disease
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
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?
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.
When you have diverticula

Diverticulosis
When the diverticula become

inflamed Diverticulitis
Intestinal Polyps Eating meat
A mass that protrudes into the lumen of the gut.
Sessile: No stalk. Just a bump.
Peduculated: Stalk. Mushroom with cap.
Non-neoplastic: Hyperplastic or metaplastic (overgrowth of goblet cells)
True neoplastic: Tubular adenoma
Peutz-Jedhers Congenital Benign, but ind. with this
polyps Hemartomatous may indicate increased risk
of other cancers.
Juvenile polyps Hemartomatous Benign Usually seen in small bowel.
Have cysts in them.
Neoplastic Tubular: Pedunculated. Not cancerous until it breaks
adenomas Malignancy depends on size through the mucosa.
Villous: Sessile and large.
Malignant potential high.
Looks like Shag rug
Tubulovillous Adenoma: Large
and malignant potential
intermediate.
Familial Polyposis Familial Adenomatous Polyposis: Hundreds of polyps (picture right)
Syndromes Gardner Syndrome: Polyps, osteomas, epidermal cysts
Rucot Syndrome: Polyps, CNS tumors (gliomas)
Hereditary Nonpolyposis Colorectal Cancer (Lynch Syndrome)
HNPCC (Lynch) AD Mutations in DNA repair Colon, endometrial, and ovarian
genes leading to cancers.
microsatellite instability Adenomas tend to be few and flat,
but occur early
Adenocarcinoma Almost exclusively in colon. Rare in small bowel.
Gastrointestinal May be from the interstitial Can occur anywhere in GI Cancer appears to arise from the TX: C-KIT/CD117 targeted
Stromal Tumors cells of Cajal. tract. MOST COMMON IN wall. treatment Gleevec
STOMACH, less common in
colon.
Carcinoid Tumors Carcinoid Syndrome: If active Appendix > Ileum > Tends to be multicentric in stomach.
and metastasize to the liver, Rectum > Stomach > Colon Usually incidental (found in pt. with
making tryptophan / Serotonin acute appendicitis).
Neurosecretory cell tumor.
Intestinal A MALToma (B-cell)
Lymphoma H. pylori associated. t(11:18)
Colon Cancer Eating meat, carbs, potatoes 60-79yo Most commonly in Cecum and
instead of ruffage. ascending colon: Bleeding, anemia,
polypoid, exophytic masses
Next common Sigmoid colon:

Obstructive symptoms. Annular,
constricting lesions.
Tumors of the Rectal May have a basaloid pattern.
Anal Canal Transitional
Squamous: Associated with HIV
and HPV
Gastrointestinal Problems in Infancy
Diaphragmatic Congenital. Symptoms are respiratory. DX: Bowel gas present in
Hernia Small intestines protrude up into Sunken/Scaphoid abdomen, thorax with hypoplastic
left chest through diaphragm. respiratory distress lungs on x-ray imaging.
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
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:
- Android (abdominal) obesity = HTN, Insulin resistance, Hyperuricemia, Dyslipoproteinemia

- Dont send someone for bariatric surgery unless their BMI > 40 or they have a disease like DM
o More effective than non-surgery to treat fatties.
o Morbidity of 20% occurs with surgery (complications)
Most common cause of death = PE.
Diarrhea
Fe, B12 deficiencies
Gallstones
Osteoporosis
- Atkins is latest best diet for losing weight, improving HDLs, TGs, and BP.
- Subjective Global Assessment via Hx and Physical is just as good at assessing malnutrition as all the expensive tests.
- Complications of Enteral (NG, NJ tube) Feeding: Aspiration (with NG), bronchopulmonary injury, diarrhea, bloating
- Complications of Parenteral (central line) feeding: Hyperglycemia, metabolic rate (problem with ppl with lung problems.)
- Refeeding Syndrome: DIE OF CARDIORESPIRATORY FAILURE.
-
Eating Disorders
Anorexia Nervosa No eating Primarily adolescent and young 6% mortality per decade TX: Family based therapy.
women. Women >>> Men Hypo K+, P-, Mg++, Alkalosis
20% Chronicity (doesnt get better)

Bulimia Nervosa Binge/Purge Bulimia will not change into Normal or high BMI
anorexia. It will stay as is. Parotid gland enlargement.
Russell sign (finger calluses)
Alcohol/drug dependency
Starvation Not getting enough Increased fat metabolism to MOST COMMON CAUSE OF DEATH =
food. conserve lean mass. PNEUMONIA
Hypercaloric feeding reverses loss

of mass.
Cachexia You got hit by a Redistribution of bodys protein Hypercaloric feeding DOESNT reverse Lasts about 7 days.
bus content Depletion of skeletal loss of lean mass. TX: FEED THEM RIGHT AWAY
muscle synthesis of acute- (Enteral or parenteral)
phase proteins Basal Energy Adaptive over short term, but it
Expenditure might kill you.
Drugs Used in GI Disorders
Drug Name MOA Pharm Profile Uses Side Effects
Antacids Weak bases that react with HCl in the Duration is limited, so Pain of ulcer and Magnesium Constipation. Mg++
Aluminum hydroxide stomach to form salt and H2O. would have to take dyspepsia. can also paralyze uterine SM.
Magnesium hydroxide them 8-10x/day to Aluminum Diarrhea
Calcium carbonate promote healing
H2 Histamine Receptor Blocks the H2 receptor in the gastric Can inhibit 70-80% acid Treat pain and Cimetidine Permanently
Antagonists -tidines parietal cells, thus cAMP, thus H+ produced in 1day. promote healing of inhibits Cyp450
Cimetidine secretion. Can be combined with ulcer Gynecomastia
Ranitidine antacids to treat pain GERD
Famotidine immediately.
PPIs - prazoles Block the H+/K+ ATPase pump which Oral Treat pain, promote Long term Higher risk of
Omeprazole normally secretes H+. Can block 90-100% H+ healing of ulcer fracture w/ chronic use (limiting
Lansoprazole production in 1day. GERD ability to absorb Ca++ from pH
Rabeprazole Most effective acid of stomach).
Pantoprazole blocker drug. Opportunistic infections.
Prostaglandin (PGE1) Enhances PGs which H+ and Peptic ulcer disease Use in caution with women since
analogs mucous/HCO3. GERD PGE1 uterine contractions.
Misoprostol NOT FOR PREGGERS.
Ammonium salt of Binds with ulcer and lays down a Oral Stress induced
Sucrose Octasulfate protective barrier. Effects stomach and ulcers in those
Sucralfate small intestine solely. mechanically
ventilated (ICU)
Prokinetic Drugs Stimulates motility of the antral and No longer on the market Gastroperesis Torsades b/c interacts with K+
Tegaserod smooth muscle of the intestine. so why did he just tell channel in heart.
us about it?
Cisapride 5-HT4 agonist Ach release
Smooth muscle contraction
Erythromycin Motilin receptor agonist Ach
release Smooth muscle contraction
Neostigmine Blocks breakdown of Ach (AchE)
Bethanechol Stimulates M3 receptor on SM cells
Metaclopramide Blocks DA reaction on D2 receptor Only short-term use Tardive dyskinesia
(normally DA inhibits Ach) which
Ach
Opioid agonists Binds to prejunctional opioids Diarrhea Constipation
Codeine receptors on cholinergic nerves to
Loperamide inhibit Ach release Paralyzes SM,
Diphenoxylate inhibits fluid secretion
Antiemetic Drugs
Drug Name MOA Pharm Profile Uses Side Effects
Metoclopramide D2 receptor antagonist (chemo-receptor
Domperidone trigger zone & Solitary n. )
Chlorpromazine Antagonists at dopamine, muscarinic, and
Prochlorpromazine histamine receptors (chemo-receptor trigger
Haloperidol zone)
Droperidol
Ondansetron 5-HT3 antagonists (stomach, small intestine)
Granisetron
Dimenhydrinate H1 and muscarinic receptor blockers Works better
Diphenhydramine (cerebellum, solitary tract nucleus) prophylactically
Meclizine
Promethazine
Scopolamine
Dronabinol Cannabanoid receptor (CB1) agonist Same receptor as MJ. Chemo-induced nausea
Lorazepam Benzodiazepine receptor agonists Anticipation/dread nausea
Alprazolam
Dexamethasone Glucocorticoid receptor agonists Mood-elevating for dread
Methylprednisilone nausea. Chemo nausea.
- Note the chemo-receptor trigger zone lies outside of
the CNS
- Marijuana is another anti-emetic drug used because
it is inhaled and is thus absorbed very rapidly.

GI - HUGE Table No Hilight PDF

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EMBRYOLOGY OF THE GI SYSTEM 3-14-11

- Buccopharyngeal membrane opens ~ 3rd week

- Families of Gut Regulatory Peptides:

OROPHARYNX AND ESOPHAGUS PHYSIOLOGY 3-14-11

STOMACH PHYSIOLOGY 3-15-11

EXOCRINE PANCREAS AND BILIARY SYSTEM PHYSIOLOGY 3-16-11

- Bile digests and helps absorption of lipids.

- Digestion: Process by which larger ingested

- 3 sites of protein digestion

- of fats are from TGs in diet.

Water Soluble Vitamins

- Absorbed through variety of mechanisms.

Water and Electrolytes

- Osmolality of a meal becomes isotonic with passage through the duodenum

- Absorbed in duodenum at a greater rate than for other divalent cations.

- Absorption increases with need (hemorrhage, growth, pregnancy)

Elecrtrolyte and Water transport in the Colon

- Cellulose, hemicelluloses, pectins, mucilages cannot be hydrolyzed by human enzymes.

Gas Accumulation in GI Tract

INTESTINAL MOTILITY 3-18-11

COLONIC MOVEMENT PATTERNS

- Colonic response to a meal is initiated by signals from the stomach and

Gastro- aka Cardiac Wet stratified squamous epithelium

Endocrine Islets of Langerhans. = Glucagon. = Insulin

Irritation Fibroma Trauma MOST COMMON SOFT TISSUE Benign proliferation of

Basically a scarring of tissue.

Peripheral Giant Cell Tons of giant cells in the tissue.

Aphthous Ulcers / Idiopathic. Necrosis of the epithelium. Ulcer. TX: Self-limited

Acute Leukemia MONOCYTIC LEUKEMIA = Swollen, bleeding gums.

Recurrent HSV First sunlight of the Especially seen in lip

Mallory-Weiss Esophageal lacerations seen in Excessive vomiting. Massive

Leiomyomas Benign, most common tumor in

Alarm Symptoms: Odynophagia, Weight loss, recurrent vomiting, intestinal

In hospital, administer NSAIDs with either Prostaglandin E analogue

RANSONS CRITERIA To eval. severity of pancreatitis

DRUGS USED IN GI DISORDERS (Notes to accompany drugs)

- H. pylori damages/colonizes the cytoprotection

Intestinal Surgery is most common Will be fine so long as

When you have diverticula

When the diverticula become

Next common Sigmoid colon:

- Android (abdominal) obesity = HTN, Insulin resistance, Hyperuricemia, Dyslipoproteinemia

20% Chronicity (doesnt get better)

Hypercaloric feeding reverses loss

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