GI Map Checklist
Human Anatomy | Human Physiology
Your GI Map is a single-page illustrated diagram -- not an outline, not a study guide written in bullet points, and not a paragraph essay. If your final product looks like a table or a numbered list, start over. The goal is a hand-drawn or digitally designed map that traces the digestive tract from mouth to anus with annotated structures, zoom-in boxes, and brief labels. Think of it as a page out of a medical atlas that you made yourself.
You are not being graded on artistic ability. Stick figures, rough sketches, and imperfect circles are completely fine. What matters is that you drew something -- a real visual representation -- not that it looks beautiful.
Every region of the GI tract should be drawn as a shape on the page -- even a simple oval or tube. From that shape, you pull out and annotate. Here are the three visual tools you should be using:
Draw a small box or circle that zooms in on a specific region. For example: draw the stomach shape, then draw a small magnified box off to the side showing the gastric gland with labeled parietal, chief, G, and D cells. Connect it to the main diagram with a line or bracket. This is how you show histology without cluttering your main diagram.
At least one region should include a small cross-section diagram showing the four histological layers -- mucosa, submucosa, muscularis externa, and serosa/adventitia -- as concentric rings or layered bands. The small intestine cross-section is a great choice: you can show villi pointing inward, label the layers, and mark where Meissner\'s and Auerbach\'s plexuses sit between the muscle layers.
Every label on your map should be a short phrase of 1-5 words, connected by an arrow to the structure it describes. Captions can be slightly longer (one sentence max) but should be written as annotations, not prose. Example: "Parietal cell -- HCl + intrinsic factor" is a good caption. A paragraph explaining the parietal cell is not.
The checklist in this tool is organized by region and category -- anatomy, histology, cells, secretions, neural, and function. Work through each region on your actual map first, then come back and check off what you included. Do not write out every checklist item as text on your map -- that defeats the purpose. Each item on this list should correspond to a label, a zoom-in box, a symbol, or an arrow on your drawing.
A good gut check: if you can fold your map and all the information is still readable as prose without the drawing, you have not made a map. You have made a document. Go back and draw.
- ✓Lips, cheeks, hard palate, soft palate, uvula
- ✓Tongue (intrinsic + extrinsic muscles) + lingual frenulum
- ✓Teeth: incisors, canines, premolars, molars
- ✓Palatine tonsils, lingual tonsils (Waldeyer\'s ring)
- ✓Stratified squamous epithelium (non-keratinized most surfaces; keratinized = gingiva, hard palate)
- ✓Taste buds on fungiform, circumvallate, and foliate papillae
- ✓Serous cells - watery enzyme-rich saliva; Mucous cells - mucin for lubrication
- ✓Salivary amylase (starch digestion), lingual lipase, lysozyme, IgA, bicarbonate
- ✓Mastication + bolus formation; chemical digestion begins (starch); taste, speech, pH buffering
- ✓Parotid - Stensen\'s duct (upper 2nd molar); CN IX. Submandibular - Wharton\'s duct; CN VII. Sublingual - ducts of Rivinus; CN VII
- ✓Parotid = purely serous; Submandibular = mixed (mostly serous); Sublingual = mostly mucous
- ✓Striated ducts modify ion content; myoepithelial cells surround acini (expel saliva)
- ✓Serous acinar cells - amylase, lysozyme, IgA; Mucous acinar cells - mucin glycoproteins
- ✓Three regions: nasopharynx, oropharynx, laryngopharynx
- ✓Pharyngeal constrictors (superior, middle, inferior) coordinate swallowing
- ✓Nasopharynx = pseudostratified ciliated columnar; Oro/laryngopharynx = stratified squamous
- ✓Deglutition: voluntary oral phase, involuntary pharyngeal + esophageal phases; epiglottis deflects to protect airway
- ✓UES (skeletal, prevents air entry); LES/cardiac sphincter (smooth, prevents GERD)
- ✓Three anatomical narrowings: cricopharyngeal, aortic arch, diaphragmatic hiatus
- ✓Stratified squamous non-keratinized epithelium (mucosa)
- ✓Muscularis: upper 1/3 skeletal, middle mixed, lower 1/3 smooth; adventitia (not serosa) in thorax
- ✓Esophageal mucous glands in submucosa for lubrication
- ✓Meissner\'s plexus (submucosal) + Auerbach\'s plexus (myenteric) present throughout; vagus CN X controls peristalsis
- ✓Peristalsis transports bolus to stomach; no digestion or absorption
- ✓Four regions: cardia, fundus, body (corpus), pylorus; greater and lesser curvature
- ✓Pyloric sphincter - controls chyme release into duodenum; angular incisure at body/pylorus junction
- ✓Rugae - longitudinal folds of mucosa/submucosa; expand to accommodate food
- ✓Simple columnar epithelium; gastric pits leading to gastric glands
- ✓Muscularis externa: THREE layers - oblique (inner), circular (middle), longitudinal (outer)Unique to stomach - enables churning and retropulsion
- ✓Serosa (visceral peritoneum) covers entire stomach
- ✓Parietal cells (oxyntic) - HCl + intrinsic factor | Fundus/body glandsHCl activates pepsinogen; intrinsic factor required for B12 absorption (ileum)
- ✓Chief cells (zymogenic) - pepsinogen + gastric lipase | Fundus/body glands
- ✓G cells - gastrin | Pyloric antrum; D cells - somatostatin; ECL cells - histamine (stimulates HCl)
- ✓Mucous neck cells + surface mucous cells - protective mucus layer against HCl
- ✓Meissner\'s plexus - glandular secretion; Auerbach\'s plexus - peristalsis and churning
- ✓Mechanical churning + chemical protein digestion; bolus converted to chyme
- ✓Limited absorption: alcohol, aspirin, lipid-soluble drugs; cephalic/gastric/intestinal secretion phases
- ✓Duodenum (~25 cm): C-shaped, retroperitoneal; ampulla of Vater + sphincter of Oddi (bile + pancreatic juice entry)
- ✓Jejunum (~2.5 m): prominent plicae circulares, thick walls, many villi
- ✓Ileum (~3.5 m): Peyer\'s patches; ileocecal valve connects to large intestine
- ✓Plicae circulares (valves of Kerckring): permanent circular folds; +3x surface area
- ✓Villi: finger-like projections with lacteal (lymphatic) core; +10x surface area
- ✓Microvilli (brush border): apical enterocyte surface; +20x SA; brush border enzymes embedded
- ✓Crypts of Lieberkuhn: intestinal glands; stem cells, Paneth cells at base
- ✓Brunner\'s glands (duodenum only): submucosal; alkaline mucus neutralizes chyme
- ✓Peyer\'s patches (ileum): submucosal lymphoid aggregates - immune surveillance
- ✓Enterocytes: brush border enzymes (maltase, sucrase, lactase, aminopeptidases); nutrient absorption
- ✓Goblet cells (mucus); Paneth cells (defensins, lysozyme - antimicrobial, crypt base)
- ✓S cells - secretin (acid chyme trigger); I cells - CCK (fat/protein trigger); K cells - GIP (glucose/fat trigger)
- ✓M cells (Peyer\'s patches): transcytose antigens to underlying lymphocytes
- ✓Meissner\'s plexus: secretion + blood flow; Auerbach\'s: peristalsis + segmentation
- ✓Duodenum: neutralizes chyme; bile + enzymes arrive; major digestion begins
- ✓Jejunum: primary absorption of carbs, proteins, fats, most vitamins and minerals
- ✓Ileum: B12 (intrinsic factor complex), bile salts (enterohepatic circulation), fat-soluble vitamins A/D/E/K
- ✓Cecum + appendix (vermiform - lymphoid tissue)
- ✓Colon: ascending, transverse (hepatic/splenic flexures), descending, sigmoid
- ✓Rectum + anal canal; internal sphincter (smooth, involuntary) + external (skeletal, voluntary)
- ✓Haustra (sacculations), teniae coli (3 longitudinal muscle bands), epiploic appendages
- ✓NO villi; flat mucosal surface with deep crypts of Lieberkuhn; abundant goblet cells
- ✓Anal canal: stratified squamous below pectinate (dentate) line; columnar above
- ✓Goblet cells: mucus for lubrication; Colonocytes: absorb water and electrolytes (Na+, Cl-, K+)
- ✓Gut microbiome: ferments fiber; produces vitamins K + B12; short-chain fatty acids
- ✓Auerbach\'s plexus: mass movements; defecation reflex: parasympathetic (pelvic splanchnic); voluntary ext. sphincter
- ✓Water and electrolyte absorption; fecal compaction and storage; microbial fermentation; vitamin synthesis
- ✓Right, left, caudate, quadrate lobes; falciform ligament; ligamentum teres
- ✓Porta hepatis: portal vein + hepatic artery + bile ducts; common hepatic duct + cystic duct = CBD --> ampulla of Vater
- ✓Dual blood supply: portal vein (75%, nutrient-rich) + hepatic artery (25%, oxygenated)
- ✓Classic hepatic lobule: hexagonal; portal triads at corners, central vein in center
- ✓Sinusoids (fenestrated endothelium); Space of Disse between sinusoids and hepatocytes
- ✓Hepatocytes: bile, albumin, clotting factors, glucose, urea, lipoproteins
- ✓Kupffer cells: macrophages in sinusoids (phagocytose bacteria, worn RBCs)
- ✓Stellate/Ito cells (Space of Disse): vitamin A storage; become fibroblasts in cirrhosis
- ✓Bile composition: bile salts (emulsify fats), bilirubin, cholesterol, phospholipids, bicarbonate
- ✓Bile production; carbohydrate/lipid/protein metabolism; detoxification; storage (glycogen, vitamins, iron); synthesis of plasma proteins and clotting factors
- ✓Fundus, body, neck; cystic duct (valves of Heister) joins common hepatic duct; lies in gallbladder fossa
- ✓Simple columnar epithelium with microvilli (absorbs water to concentrate bile up to 10x)
- ✓No submucosa or muscularis mucosae; Rokitansky-Aschoff sinuses (mucosal outpouchings)
- ✓Stores and concentrates bile; releases into CBD when CCK is secreted (fat in duodenum)
- ✓Head (duodenal C-loop), neck, body, tail (spleen); mostly retroperitoneal
- ✓Duct of Wirsung (main) + Santorini (accessory); join CBD at ampulla of Vater
- ✓Exocrine (~95%): serous acini of acinar cells; centroacinar cells lining duct lumen
- ✓Endocrine (~5%): islets of Langerhans scattered among acini
- ✓Acinar cells: amylase, lipase, trypsinogen, chymotrypsinogen, elastase, phospholipase A2 | Stimulated by CCK
- ✓Centroacinar cells: bicarbonate-rich fluid | Stimulated by secretin
- ✓Alpha cells - glucagon; Beta cells - insulin (most numerous); Delta cells - somatostatin; PP cells - pancreatic polypeptide
- ✓Exocrine: neutralizes acid chyme (bicarbonate); digests all macronutrients (enzymes)
- ✓Endocrine: insulin/glucagon regulate blood glucose; somatostatin modulates both
- ✓Meissner\'s plexus (submucosal): between mucosa and inner circular muscleControls: glandular secretion, mucosal blood flow, sensory detection of luminal contents
- ✓Auerbach\'s plexus (myenteric): between inner circular and outer longitudinal muscleControls: peristalsis, segmentation, GI smooth muscle tone (motility)
- ✓ENS: ~500 million neurons; functions independently of CNS
- ✓Parasympathetic (vagus CN X / pelvic splanchnic): stimulates motility and secretion
- ✓Sympathetic (celiac, sup/inf mesenteric ganglia): inhibits motility; vasoconstriction
- ✓Peristalsis reflex: stretch detected, circular muscle contracts behind bolus, relaxes ahead (law of the intestine)
Rubric | 50 pts Total
- ✓Cephalic PhaseONSight, smell, taste, or thought of food; mediated entirely by vagus nerve (CN X) before food arrivesEFFECTStimulates gastric glands (HCl, pepsinogen, mucus); ACh from vagus also stimulates G cells to release gastrinOFFRemoval of sensory stimulus; rising acid pH; somatostatin from D cellsLINKWhy hunger and anticipation cause "stomach growling" -- entirely neural, no food required
- ✓Gastric PhaseONStomach distension (stretch receptors); peptides and amino acids; rising pH as food buffers acidEFFECTLocal myenteric reflexes + vagovagal reflexes stimulate G cells (gastrin) and ECL cells (histamine) -- massive HCl and pepsinogen amplificationOFFpH falls below 3: somatostatin (D cells) inhibits G cells; secretin from duodenum inhibits gastrin once chyme exitsLINKGastrin also increases LES tone and stimulates motility -- one hormone, multiple coordinated effects
- ✓Intestinal PhaseONAcid chyme entering duodenum; fats and proteins; osmolarity and distension of duodenal wallEFFECTReleases secretin (neutralize acid) and CCK (digest fats/proteins); enterogastric reflex slows gastric emptyingOFFRising duodenal pH removes secretin stimulus; fat digestion removes CCK stimulus; gastric emptying slows automaticallyLINKIntestinal phase is INHIBITORY to the stomach -- protects the duodenum from acid chyme overload
- ✓Gastrin -- G cells, pyloric antrumONPeptides/amino acids in stomach; vagal ACh (cephalic phase); stomach distension; rising pH (food buffers acid)EFFECTStimulates parietal cells (HCl); chief cells (pepsinogen); increases LES tone; promotes motility; stimulates ECL cells (histamine)OFFpH < 3 directly inhibits G cells; somatostatin (D cells); secretin from duodenum
- ✓Secretin -- S cells, duodenumONAcid chyme in duodenum (pH < 4.5); fatty acids in duodenumEFFECTPancreatic centroacinar cells secrete bicarbonate (neutralizes acid); inhibits gastric acid; inhibits gastrin; stimulates bile flow from liverOFFRising duodenal pH removes the acid stimulus -- self-resolving negative feedbackLINKDraw the acid-bicarbonate seesaw: parietal cell HCl --> duodenum pH drops --> secretin --> pancreatic HCO3- --> pH rises --> secretin stops
- ✓CCK (Cholecystokinin) -- I cells, duodenum/jejunumONFats (fatty acids, monoglycerides) and proteins (peptides, amino acids) in duodenumEFFECTGallbladder contraction (bile release); pancreatic acinar enzymes; relaxes sphincter of Oddi; inhibits gastric emptying; satiety signal to hypothalamusOFFDigestion of fats/proteins removes duodenal stimulus; trypsin cleaves CCK-releasing factorLINKCCK coordinates THREE organs simultaneously: stomach (slow), gallbladder (contract), pancreas (release enzymes). Draw all three arrows from one I cell.
- ✓GIP (Glucose-dependent Insulinotropic Peptide) -- K cells, duodenum/jejunumONGlucose and fats in the duodenum (after a mixed meal)EFFECTInhibits gastric acid and motility; stimulates insulin from pancreatic beta cells (incretin effect)OFFFalling blood glucose; glucose absorption removes duodenal stimulusLINKIncretin effect: oral glucose causes more insulin release than IV glucose because the gut signals the pancreas in advance
- ✓Motilin -- M cells, duodenum/jejunumONFasting state; released cyclically every 90-120 minutes between mealsEFFECTInitiates migrating motor complex (MMC): powerful peristaltic waves sweep residue from stomach through SI -- "intestinal housekeeper"OFFFood intake; secretin and CCK released after eating suppress the MMCLINKBorborygmi (stomach growling when hungry) = motilin-driven MMC. Erythromycin is a motilin agonist used for gastroparesis.
- ✓Somatostatin -- D cells (stomach, pancreas, intestine)ONLow gastric pH; high blood glucose; fat/protein in gut -- generally "too much" of any GI stimulusEFFECTInhibits virtually everything: gastrin, secretin, CCK, GIP, insulin, glucagon, HCl, pancreatic enzymes, GI motility. The master brake of the GI system.OFFRemoval of stimulus; vagal stimulation can suppress D cell activityLINKSomatostatin acts PARACRINE (on neighboring cells, not through blood). D cells are positioned beside G cells, parietal cells, and beta cells to provide local inhibition. Draw short local arrows.
- ✓Pepsinogen -- Pepsin cascade (stomach)ONChief cells release pepsinogen (inactive); HCl drops luminal pH below 2EFFECTLow pH cleaves pepsinogen --> pepsin; pepsin then autocatalytically activates more pepsinogen; cleaves peptide bonds in proteinsOFFpH rises above 5: pepsin irreversibly inactivated; bicarbonate in duodenum immediately deactivates pepsin when chyme arrivesLINKDraw the autocatalytic loop with a note: "self-amplifying but pH-dependent." Why proenzymes? Premature activation would digest the cell that made them.
- ✓Trypsinogen -- Trypsin cascade (duodenum)ONPancreas secretes trypsinogen; enteropeptidase (enterokinase) on duodenal brush border cleaves it to trypsinEFFECTTrypsin activates itself (autocatalysis) AND activates chymotrypsinogen, proelastase, procarboxypeptidases, phospholipase A2. Trypsin = "master activator" of all pancreatic proenzymes.OFFPancreatic secretory trypsin inhibitor (PSTI) prevents premature activation inside the gland; no enteropeptidase outside the duodenumLINKDraw the cascade tree: enterokinase --> trypsin --> everything else. In pancreatitis: premature intrapancreatic activation --> autodigestion.
- ✓Brush Border Enzyme Digestion (small intestine)ONSubstrate contacts enterocyte apical membrane (physical contact required -- these enzymes are NOT secreted into the lumen)EFFECTMaltase: maltose --> 2 glucose. Sucrase: sucrose --> glucose + fructose. Lactase: lactose --> glucose + galactose. Aminopeptidases: complete protein digestion at cell surface.OFFNo substrate = no activity; enzyme expression can be reduced (lactase decline in adults = lactose intolerance)LINKFinal digestion happens AT the cell surface, not in the lumen. Draw a tiny enterocyte with enzymes sticking out of the brush border, products entering the cell.
- ✓Bile Release and EmulsificationONFat in duodenum --> I cells release CCK; vagal stimulation also promotes gallbladder contractionEFFECTGallbladder contracts + sphincter of Oddi relaxes; bile salts emulsify fat globules into tiny droplets; dramatically increases surface area for pancreatic lipaseOFFFat digestion and absorption removes CCK stimulus; gallbladder relaxes
- ✓Micelle Formation and Fat AbsorptionONPancreatic lipase cleaves triglycerides --> monoglycerides + fatty acids; bile salts aggregate around productsEFFECTMicelles ferry lipids to enterocyte brush border; lipids diffuse across membrane; reassembled into triglycerides inside cell; packaged into chylomicrons; secreted into lacteals (lymph, not portal blood)OFFShort/medium-chain FAs bypass lacteals and go directly to portal blood
- ✓Enterohepatic Circulation of Bile SaltsONBile salts reach terminal ileum after participating in fat digestionEFFECT~95% of bile salts actively reabsorbed in terminal ileum; enter portal blood; returned to liver; re-secreted into bile -- recycled 2-3x per mealOFF~5% lost in feces; liver synthesizes new bile salts from cholesterol to replace lossesLINKDraw the full loop: liver --> bile duct --> duodenum --> jejunum (micelles) --> ileum (reabsorbed) --> portal vein --> liver. Ileal disease (Crohn\'s) breaks this loop --> fat malabsorption.
- ✓Peristalsis Reflex -- Law of the IntestineONDistension of the gut wall activates intrinsic primary afferent neurons (IPANs)EFFECTAscending excitation (ACh): circular muscle contracts BEHIND the bolus. Descending inhibition (VIP, NO): circular muscle relaxes AHEAD of bolus. Net = propulsion.LINKDraw two arrows at any gut segment: "+" ACh behind, "-" VIP/NO ahead. Label: ascending excitation / descending inhibition.
- ✓Segmentation vs. PeristalsisONSegmentation: pacemaker cells in circular muscle; dominant in SI during active digestion. Peristalsis: dominant in esophagus always; SI between meals (MMC).EFFECTSegmentation MIXES chyme with juices and maximizes contact time with absorptive surface (no net movement). Peristalsis PROPELS bolus forward.LINKParasympathetic favors both; Sympathetic inhibits both. Draw the ANS balance beam: "rest and digest" vs. "fight or flight."
- ✓Gastroileal and Gastrocolic ReflexesONFood entering the stomach (distension and chemical stimulation)EFFECTGastroileal reflex: relaxes ileocecal valve (chyme from ileum --> cecum). Gastrocolic reflex: mass movements in large intestine -- why eating causes urge to defecate.LINKDraw a long reflex arc: stomach --> ileocecal valve and stomach --> colon. Mediated by vagus + ENS reflexes + gastrin/serotonin.
- ✓Insulin Secretion -- Beta cellsONRising blood glucose (ATP closes K+ channel, depolarization, Ca2+ entry); GIP and GLP-1 incretins from gut; vagal ACh; amino acidsEFFECTGLUT4 translocated to surface in muscle and adipose (glucose uptake); glycogen synthesis; fat storage; protein synthesis; inhibits gluconeogenesis and lipolysisOFFFalling blood glucose; somatostatin (D cells); sympathetic stimulation suppresses insulinLINKIncretin loop: food in duodenum --> GIP/GLP-1 --> beta cells release insulin BEFORE glucose even peaks in blood. The gut anticipates the glucose load.
- ✓Glucagon Secretion -- Alpha cellsONFalling blood glucose; amino acids (protein-only meal); sympathetic stimulation; cortisolEFFECTGlycogenolysis: liver glycogen --> glucose. Gluconeogenesis: liver makes new glucose. Lipolysis: fat breakdown. Net: raises blood glucose.OFFRising blood glucose; insulin (beta cells inhibit alpha cells paracrine); somatostatinLINKDraw the insulin-glucagon seesaw. High glucose --> insulin up, glucagon down. Low glucose --> glucagon up, insulin down. Somatostatin sits at the fulcrum inhibiting both.
- ✓Acid-Bicarbonate Feedback LoopMAP ITParietal cell --> HCl --> duodenum pH drops --> S cells release secretin --> pancreas secretes HCO3- --> pH rises --> secretin stops. Draw as a closed circle with + and - arrows.
- ✓Gastrin Negative Feedback LoopMAP ITG cell --(gastrin)--> parietal cell --(HCl, pH drops)--> D cell --(somatostatin)--> inhibits G cell. A tiny 3-cell loop with +/- arrows is all you need.
- ✓CCK Three-Target Integration MapMAP ITI cell --> CCK --> [1] gallbladder contracts + [2] pancreatic enzymes released + [3] gastric emptying slows. One source, three arrows, three targets.
- ✓Enterohepatic Circulation CircuitMAP ITLiver makes bile salts --> gallbladder stores --> duodenum (bile released) --> jejunum (micelles, fat absorption) --> ileum (95% reabsorbed) --> portal vein --> liver. Draw as a full loop with arrows.
- ✓Insulin-Glucagon SeesawMAP ITDraw a balance beam. Left: HIGH glucose --> insulin up, glucagon down. Right: LOW glucose --> glucagon up, insulin down. Somatostatin sits above the fulcrum, inhibiting both simultaneously.