Click any card to flip · 22 Step 1 high-yield concepts0 / 22 seen
LO 1 — SI Anatomy: Villi & Microvilli
Structure, function, and surface area amplification?
Answer
Villi: Finger-like projections of mucosa (lamina propria core + epithelium) Microvilli: Brush border on apical surface of enterocytes; 1 μm tall Surface area: ~300× amplification (300 m²) for absorption Contents: Lacteals (chylomicron uptake), crypts of Lieberkühn (stem cells/goblet cells)
LO 2 — Unstirred Water Layer
What is it; why rate-limiting for lipophilic drugs; clinical relevance?
Answer
Definition: Stagnant fluid layer between brush border and intestinal lumen; ~200 μm thick Mechanism: Fatty acids/monoglycerides must diffuse through aqueous layer → dissolved micelles slower than glucose Rate-limiting step: Constrains lipid absorption rate (not brush border)
LO 3 — Digestive Enzymes: Salivary Amylase
Location, substrate, product, and what percentage of starch digestion?
Answer
Source: Salivary glands (serous cells) Action: Hydrolyzes α-1,4 glycosidic bonds in starch → maltose + limit dextrins Contribution: ~30% of starch digestion; inactivated by stomach acid Step 1 note: Minimal absorption in mouth; most work in small intestine via pancreatic amylase
LO 4 — Brush Border Enzymes
Location and three key disaccharidases for final carb digestion?
Answer
Site: Apical membrane of enterocytes (brush border) Enzymes: Lactase (lactose→glucose+galactose), sucrase (sucrose→glucose+fructose), maltase (maltose→glucose+glucose) Product: Monosaccharides ready for transport Step 1 trap: Lactase deficiency → ↓ activity → osmotic diarrhea
LO 5 — SGLT1 Transporter
Mechanism, substrates, and why it matters for glucose/galactose absorption?
Answer
Type: Secondary active transport (Na⁺-glucose cotransporter) Substrates: Glucose + galactose + Na⁺ (1:1:1 stoichiometry) Energy: Driven by Na⁺ gradient (maintained by Na⁺/K⁺-ATPase) Location: Apical membrane of enterocytes Clinical: Oral rehydration therapy exploits SGLT1 coupling
LO 6 — Cellulose & β-1,4 Linkage
Why humans cannot digest cellulose; the consequence?
Mechanism of trypsin activation; why this is crucial?
Answer
Trypsinogen: Inactive protease from pancreas Enterokinase: Brush border enzyme that cleaves trypsinogen → active trypsin Amplification: Trypsin then auto-activates more trypsinogen + activates other pancreatic zymogens Critical: Missing enterokinase → no protease activation → protein malabsorption
LO 10 — PepT1 & Amino Acid Transport
PepT1 mechanism and location; final absorption of amino acids?
Source, substrate, and percentage of lipid digestion; clinical significance?
Answer
Source: Gastric mucosa (chief cells) Action: Hydrolyzes triglycerides → 2-monoglyceride + fatty acids (mainly short/medium chain) Contribution: ~10-30% of lipid digestion; acid-stable Clinical: Patients with pancreatic insufficiency still digest some fat via gastric lipase
LO 12 — Pancreatic Lipase & Colipase
Mechanism of lipase action; role of colipase; final products?
Answer
Pancreatic lipase: Cleaves triglycerides → 2-monoglyceride + 2 fatty acids Colipase: Cofactor that anchors lipase to triglyceride droplet surface (aids emulsification) Site: Acts on bile salt-emulsified fat in SI lumen Efficiency: Most lipid digestion (70-90%)
LO 13 — Micelle Formation & CMC
Structure of micelles; role of bile salts; critical micellar concentration?
Answer
Micelle: Aggregates of fatty acids + monoglycerides + bile salts in SI lumen Bile salt: Amphipathic (hydrophobic + hydrophilic); arranges with lipids in center, hydrophilic side out CMC: ~2-20 mM; below this, no micelles form → poor lipid absorption Function: Keeps lipid products soluble in aqueous lumen; delivers to brush border via unstirred layer
LO 14 — Chylomicron Assembly
Site of assembly; protein carriers; role of MTP; how they exit?
Answer
Site: Enterocyte SER (smooth endoplasmic reticulum) Core: Re-esterified triglycerides + cholesterol esters + fat-soluble vitamins Coat: apoB-48 (N-terminal fragment of apoB) + apoA-I, apoC-II, apoE MTP: Microsomal triglyceride transfer protein assembles lipid core onto apoB-48 Exit: Exocytosis → lacteal (lymphatic) → thoracic duct → blood
LO 15 — Abetalipoproteinemia
Gene defect; pathophysiology; clinical triad?
Answer
Defect: Mutation in MTP gene → absent chylomicrons/VLDL assembly Pathophysiology: Fat-soluble vitamins (A, D, E, K) accumulate in enterocytes → cannot absorb lipids Clinical triad: (1) Steatorrhea (fatty stools); (2) Acanthocytes (spiky RBCs); (3) Neurological (ataxia, night blindness from vitamin E deficiency) Management: High-dose fat-soluble vitamins (especially vitamin E)
LO 16 — Enterohepatic Circulation
Pathway of bile acid recycling; reabsorption site; efficiency?
Answer
Pathway: Bile acids secreted → emulsify lipids → reabsorbed at terminal ileum (ASBT transporter) → return to liver via portal blood Efficiency: ~95% recycled per cycle; ~6-8 cycles/day Consequence: Only ~0.5 g/day lost in feces; liver must synthesize replacement Clinical: Ileal resection → bile acid loss → steatorrhea + cholestasis
LO 17 — Ileal Resection Consequences
What is lost; effects on vitamins and bile acids; gallstone risk?
Answer
Loss of: Terminal ileum (B12 absorption site, bile acid reabsorption site) Bile acid: Malabsorption → steatorrhea + fat-soluble vitamin deficiency (ADEK) Vitamin B12: Must bind intrinsic factor (parietal cells) then absorbed in terminal ileum → deficiency within 2-3 years Gallstones: ↓ bile acids → ↑ cholesterol saturation → stone formation
LO 18 — Sodium Absorption: Three Routes
Jejunal, ileal, and colonic Na absorption mechanisms?
Answer
Jejunum: Coupled to glucose (SGLT1) or amino acids (Na/H exchanger) Ileum: Na/Cl cotransporter (electroneutral) Colon: ENaC (epithelial Na channel, aldosterone-regulated) Clinical: Aldosterone ↑ colonic Na reabsorption (compensate for proximal loss)
LO 19 — Iron Transport: DcytB & DMT1
Reduction step; transporter; regulation by hepcidin?
Answer
DcytB: Duodenal cytochrome b reductase reduces ferric (Fe³⁺) → ferrous (Fe²⁺) DMT1: Divalent metal transporter 1 carries Fe²⁺ (+ Mn, Zn, Pb) into enterocyte Storage: Ferritin; export via ferroportin Hepcidin: Hormone ↑ in iron overload; binds ferroportin → degradation → ↓ iron export (trap in enterocytes)
LO 20 — Calcium Transport: Vitamin D Role
Calbindin-D9k; duodenal vs. jejunal mechanism; vitamin D regulation?
Answer
Duodenum: Primary site; transcellular (active); requires calbindin-D9k (vitamin D-dependent protein) Jejunum: Secondary; paracellular (passive) through tight junctions Regulation: 1,25-vitamin D upregulates calbindin + apical Ca²⁺ channels + CaSR Clinical: Vitamin D deficiency → ↓ duodenal Ca absorption → hypocalcemia
LO 21 — Vitamin B12 Absorption
Intrinsic factor role; site of absorption; transporters?
Answer
IF: Glycoprotein from parietal cells binds B12 (cyanocobalamin) → stable complex Transport: IF-B12 → terminal ileum (specific receptor on enterocytes) Transcobalamin II: Binds B12 in blood for delivery to tissues Clinical: Pernicious anemia (IF deficiency), ileal Crohn's, or ileal resection → B12 malabsorption
LO 22 — Colonic Diarrhea: Osmotic vs. Secretory
Mechanism of each; fasting response; electrolyte profile?
Answer
Osmotic: Unabsorbed solute (lactose, sorbitol) → osmotic gradient → water follows → STOPS with fasting Secretory: ↑ cAMP/cGMP (cholera toxin, VIP) → ↑ Cl⁻ secretion via CFTR → water follows → CONTINUES with fasting Stool Na: Osmotic diarrhea has low stool Na (poor reabsorption); secretory has elevated Na
Put-in-Sequence Drills
Carbohydrate Digestion Cascade
Order the steps of starch digestion from lumen to monosaccharide absorption.
Micelles form (fatty acids + monoglycerides + bile salts) → delivery through unstirred layer
Absorption at brush border → re-esterification in SER → chylomicron assembly + exocytosis
Bile Acid Enterohepatic Circulation
Trace bile acid recycling from liver to terminal ileum and back.
Bile acids synthesized from cholesterol in liver
Stored in gallbladder; released with meal into duodenum
Emulsify lipids throughout SI; enter terminal ileum
ASBT transporter reabsorbs 95% at terminal ileum
Portal blood return to liver; recycled 6-8 times/day
Bile acids synthesized from cholesterol in liver
Stored in gallbladder; released with meal into duodenum
Emulsify lipids throughout SI; enter terminal ileum
ASBT transporter reabsorbs 95% at terminal ileum
Portal blood return to liver; recycled 6-8 times/day
Micronutrient Absorption Pathways
Order iron, calcium, and vitamin B12 absorption from lumen to blood.
Iron: DcytB reduces Fe³⁺ → Fe²⁺; DMT1 transports into enterocyte
Calcium: 1,25-vitamin D upregulates calbindin + CaSR; duodenal transcellular absorption
B12: Parietal cell IF binds cyanocobalamin → IF-B12 complex to terminal ileum
Terminal ileum: ASBT-mediated B12 reabsorption; Fe transported via ferroportin
Transcobalamin II, transferrin carriers in blood transport to tissues
Iron: DcytB reduces Fe³⁺ → Fe²⁺; DMT1 transports into enterocyte
Calcium: 1,25-vitamin D upregulates calbindin + CaSR; duodenal transcellular absorption
B12: Parietal cell IF binds cyanocobalamin → IF-B12 complex to terminal ileum
Terminal ileum: ASBT-mediated B12 reabsorption; Fe transported via ferroportin
Transcobalamin II, transferrin carriers in blood transport to tissues
Single Best Answer Questions
MCQ 1
A 42-year-old man with celiac disease has villous atrophy on small bowel biopsy. Which of the following best explains his steatorrhea?
A Decreased lipase secretion from pancreas
B Reduced absorptive surface area and brush border enzyme deficiency
C Decreased cholecystokinin (CCK) secretion
D Impaired bile acid synthesis in liver
E Increased bacterial overgrowth in terminal ileum
Answer: B Celiac disease → villous atrophy → loss of brush border enzymes + absorptive surface area. Both lipid AND carbohydrate absorption suffer. A is incorrect (pancreas function intact); C is incorrect (CCK actually ↑ to try to compensate); D is incorrect (liver normally makes bile acids); E is incorrect (not primary mechanism).
MCQ 2
A 3-year-old presents with osmotic diarrhea, bloating, and abdominal discomfort after drinking milk. H₂ breath test shows elevated hydrogen after lactose challenge. Which mechanism best explains the osmotic diarrhea?
A Enterotoxin-mediated CFTR activation
B Undigested lactose draws water into intestinal lumen
C Villous atrophy reducing absorptive surface
D Decreased pancreatic enzyme secretion
E Bacterial translocation into lamina propria
Answer: B Lactase deficiency → undigested lactose → osmotic effect (water follows solute). The H₂ breath test confirms undigested lactose fermentation by colon bacteria. A is secretory (cholera-type); C is malabsorptive; D and E are not mechanisms of lactase deficiency.
MCQ 3
A neonate has severe steatorrhea, acanthocytes on blood smear, and progressive ataxia. MRI shows cerebellar atrophy. Genetic testing reveals MTP gene mutation. Which of the following best explains this presentation?
A Abetalipoproteinemia — cannot assemble chylomicrons or VLDL
B Familial hypercholesterolemia — LDL receptor deficiency
C Tangier disease — apoA-I deficiency
D Niemann-Pick disease — sphingomyelinase deficiency
E Gaucher disease — glucocerebrosidase deficiency
Answer: A MTP (microsomal triglyceride transfer protein) assembles chylomicrons. Loss of MTP → absent lipoproteins → malabsorption of fat AND fat-soluble vitamins (especially vitamin E) → acanthocytes + neurological symptoms (ataxia). B-E do not involve MTP mutations or this clinical triad.
MCQ 4
A 55-year-old man with Crohn's disease undergoes 2 meters of terminal ileum resection. Which complication is most likely to occur first?
A Vitamin B12 deficiency (pernicious anemia)
B Fat-soluble vitamin deficiency (ADEK)
C Bile acid malabsorption and steatorrhea
D Gallstone formation
E Hyperoxaluria and renal stone formation
Answer: C Terminal ileum = site of BOTH B12 absorption AND bile acid reabsorption. Bile acid loss occurs immediately (95% normally reabsorbed here) → steatorrhea + fat malabsorption. B12 depletion takes 2-3 years (body stores last ~1 year). Gallstones develop later (from bile acid loss). A occurs but takes months. D-E are secondary consequences.
MCQ 5
A 7-year-old with chronic diarrhea has normal stool osmolality and osmotic gap <50 mOsm/kg despite fasting. Stool chloride is elevated. Which best explains the underlying pathophysiology?
A Osmotic diarrhea from unabsorbed lactose
B Secretory diarrhea from elevated intracellular cAMP
C Villous atrophy reducing surface area
D Excessive colonic fermentation
E Increased bacterial translocation
Answer: B Secretory diarrhea: low osmotic gap + elevated stool Cl⁻ + persists with fasting (indicates ion secretion, not osmotic effect). Caused by toxins (cholera) or neuroendocrine tumors (↑cAMP/cGMP) activating CFTR. A has high osmotic gap; C is malabsorptive; D and E not primary mechanisms.
MCQ 6
A 35-year-old with iron deficiency anemia is found to have achlorhydria and lack of intrinsic factor (IF). Which of the following is the most specific explanation?
A Atrophic gastritis from chronic H. pylori infection
C Autoimmune attack on parietal cells (pernicious anemia)
D Zollinger-Ellison syndrome
E Pancreatic insufficiency
B Celiac disease with villous atrophy
Answer: C Pernicious anemia = autoimmune destruction of parietal cells → loss of both HCl (achlorhydria) AND IF (B12 malabsorption). If due to H. pylori (A), typically HCl preserved in non-fundal areas. B affects duodenum not gastric mucosa. D/E cause different patterns.
MCQ 7
A patient has severe protein malabsorption despite normal pancreatic enzymes and intact small bowel. Genetic testing reveals defects in the neutral amino acid transporter. Which genetic syndrome is this?
A Hartnup disease
B Cystinuria
C Familial hypercholesterolemia
D Primary hyperparathyroidism
E Wilson disease
Answer: A Hartnup disease = defect in neutral amino acid transporter (basolateral exit) → amino acid malabsorption + pellagra (tryptophan deficiency → low niacin). Cystinuria (B) affects basic + dibasic amino acids. C, D, E are unrelated lipid/mineral disorders.
MCQ 8
Oral rehydration therapy (ORT) with glucose + sodium + water is effective in cholera because:
A Glucose inhibits CFTR-mediated chloride secretion
B Sodium and glucose cotransport via SGLT1 creates osmotic gradient to reabsorb water
C Glucose downregulates cholera toxin production
D Sodium blocks bacterial invasion of epithelial cells
E Glucose provides ATP for Na⁺/K⁺-ATPase to pump out excess intracellular sodium
Answer: B Cholera toxin causes secretory diarrhea (↑Cl⁻ loss), but SGLT1 (coupled Na⁺/glucose uptake) remains functional. ORT exploits this: glucose-coupled Na absorption pulls water back into blood by osmosis. A is incorrect (CFTR still active); C/D are incorrect (doesn't affect toxin); E is incomplete mechanism.
MCQ 9
A 50-year-old woman with history of pancreatic cancer develops steatorrhea. Which of the following pancreatic products is MOST critical for fat digestion in the duodenum?
A Trypsinogen
B Amylase
C Colipase
D Bicarbonate
E Carboxypeptidase
Answer: C Colipase is the essential cofactor for pancreatic lipase. Without colipase, lipase cannot anchor to triglyceride droplets → no digestion. A is for protein; B for carbs; D neutralizes stomach acid (needed for environment but not directly for lipase); E is proteolysis.
MCQ 10
A 25-year-old woman presents with night blindness and progressive ataxia. Serum retinol is low. She is found to have steatorrhea and absent chylomicrons on lipoprotein electrophoresis. Which transport protein is deficient?
A Albumin
B Retinol-binding protein (RBP)
C Apolipoprotein B-48
D Transcobalamin II
E Intrinsic factor
Answer: C Absent chylomicrons + night blindness (vitamin A deficiency) + ataxia (vitamin E deficiency) → abetalipoproteinemia. ApoB-48 is the N-terminal fragment of apoB that forms the structural protein of chylomicrons. Without it, no lipoprotein assembly. A, B, D, E are unrelated to lipoprotein formation.
Clinical Vignette MCQ
Vignette 1
A 4-year-old boy is brought to the pediatrician with chronic diarrhea and abdominal bloating after eating dairy products. His growth is normal. He has had frequent respiratory infections but no fever. Stool osmolality is 280 mOsm/kg (elevated). On physical exam, he has no rash or edema. Labs show normal serum albumin and hemoglobin. H₂ breath test done after lactose challenge shows marked elevation of H₂.
A Celiac disease with villous atrophy
B Primary lactase deficiency
C Tropical sprue
D Whipple disease (T. whipplei)
E Cystic fibrosis
Answer: B Lactase deficiency: osmotic diarrhea (elevated osmolality) + bloating + elevated H₂ breath test (undigested lactose → bacterial fermentation). Normal growth/albumin rules out celiac (A, C would show malabsorption). D requires fever/arthralgias. E would have elevated sweat chloride + pancreatic insufficiency.
Vignette 2
A 28-year-old man with severe Crohn's disease undergoes 1.5 meters of terminal ileum resection. He recovers well from surgery. At 6 months postop, he presents with fatigue and paresthesias. Labs show low serum B12 and elevated methylmalonic acid. His serum folate is normal. He also has diarrhea with fatty stools.
A Pernicious anemia from autoimmune parietal cell destruction
B Folate deficiency with secondary B12 elevation
C B12 malabsorption from loss of terminal ileum absorption site
D Bacterial overgrowth consuming B12 in proximal intestine
E Increased B12 requirement from hypermetabolism post-surgery
Answer: C Terminal ileum removed → site of IF-B12 complex absorption gone → B12 malabsorption (develops in 2-3 years as stores deplete). Elevated methylmalonic acid confirms B12 deficiency (different from folate). Fatty stools from concurrent bile acid malabsorption (also absorbed in terminal ileum). A would have achlorhydria/anti-IF antibodies. B/D/E incorrect.
Vignette 3
A 6-month-old girl presents with severe steatorrhea (fatty, foul-smelling stools), failure to thrive, and developmental delay. On exam, she has nystagmus and ataxia. Serum retinol and tocopherol are both low. Blood smear shows acanthocytes. Abdominal ultrasound shows normal pancreas and liver. Genetic testing reveals a mutation in the MTP gene.
A Pancreatic insufficiency from cystic fibrosis
B Abetalipoproteinemia from MTP mutation
C Celiac disease with severe villous atrophy
D Tangier disease from apoA-I deficiency
E Familial hypobetalipoproteinemia
Answer: B Classic abetalipoproteinemia: MTP mutation → no chylomicron assembly → steatorrhea + fat-soluble vitamin deficiency (retinol + tocopherol low) + acanthocytes + neurological symptoms (ataxia, nystagmus). Normal pancreas/liver rules out A. C would show villous atrophy on biopsy. D/E different lipid disorders.
Vignette 4
A 35-year-old man from rural Guatemala presents with chronic diarrhea, weight loss, arthralgias, and fever. He has a prolonged PT and low albumin. Small bowel biopsy shows lamina propria filled with macrophages that stain positive with PAS stain and are diastase-resistant. Blood cultures are negative.
A Tropical sprue from unknown infectious agent
B Whipple disease from Tropheryma whipplei
C Crohn disease with suppurative granulomas
D Intestinal tuberculosis from M. tuberculosis
E MAC infection in advanced HIV
Answer: B Whipple disease: Tropheryma whipplei (Gram-positive rod) → PAS+ (periodic acid-Schiff) macrophages in lamina propria (diastase-resistant = glycoprotein cell wall). Malabsorption + systemic symptoms (fever, arthralgias) + geographic risk (tropical). A has villous atrophy not macrophage infiltration. C/D/E have different histology.
Vignette 5
A 22-year-old medical student presents with diarrhea that began after a trip to India 2 weeks ago. She has mild dehydration and low-grade fever. Stool is watery and culture grows Vibrio cholerae. She is given IV fluids and a solution of glucose + sodium + water (ORT). Her symptoms resolve within 3 days without antibiotics.
A Osmotic diarrhea from undigested carbohydrates
B Secretory diarrhea from cholera toxin-induced CFTR activation
C Malabsorptive diarrhea from villous destruction
D Inflammatory diarrhea from neutrophil infiltration
E Motility diarrhea from serotonin hypersecretion
Answer: B Cholera toxin → ADP-ribosylates Gs protein → ↑cAMP → ↑Cl⁻ secretion via CFTR (secretory diarrhea, continues with fasting). ORT effective because SGLT1 (Na-glucose cotransport) still works → water reabsorbed. A is osmotic (stops fasting). C/D/E incorrect mechanisms for cholera.
Step 1 Trap Concepts
Trap 1
"Lactose intolerance means the patient has celiac disease."
WRONG. Lactase deficiency (primary, secondary, or congenital) causes osmotic diarrhea. Celiac disease = autoimmune villous atrophy affecting ALL brush border enzymes + nutrients. Celiac causes both lactose AND other disaccharide malabsorption. Lactase deficiency is isolated enzyme loss. Different mechanisms, different treatments.
Trap 2
"SGLT1 transporter works for all monosaccharides equally."
WRONG. SGLT1 = secondary active, carries glucose + galactose + Na⁺. Fructose uses GLUT5 (facilitated, no Na coupling). All exit basolateral via GLUT2. Students confuse this on questions about fructose malabsorption (GLUT5 deficiency causes bloating but NOT glucose/galactose problems).
Trap 3
"Steatorrhea in pancreatic insufficiency is because lipase is completely absent."
WRONG. Even with severe pancreatic insufficiency, gastric lipase (10-30% of digestion) still works. Also, patients can absorb some medium-chain triglycerides via different mechanism. But MORE importantly: colipase is often the limiting factor — lipase needs colipase to anchor to fat droplets. Absent colipase = total lipase failure.
Trap 4
"Bile acids are needed for fat digestion, not absorption."
WRONG. Bile acids: (1) Emulsify fat droplets (aid pancreatic lipase) AND (2) Form micelles that solubilize lipid products through unstirred layer → delivery to brush border. Without micelles, even though lipase digests fats, the products can't reach the enterocyte. Both digestion AND absorption require bile acids.
WRONG. Terminal ileum = SITE of absorption, not storage. Body stores B12 in liver (~1-2 year supply). Ileal resection → immediate malabsorption, but symptoms take 2-3 years. Bile acid loss (also absorbed in terminal ileum) causes steatorrhea IMMEDIATELY. Know the timeline: bile acids → weeks, B12 → years.
Trap 6
"Osmotic diarrhea continues when the patient fasts, while secretory diarrhea stops."
WRONG — REVERSED! Osmotic diarrhea (unabsorbed solute) STOPS with fasting (no solute intake = no osmotic gradient). Secretory diarrhea (active ion secretion like cholera toxin) CONTINUES because it's not solute-dependent. This is a classic Step 1 reversal trap. Always think: "fasting test" differentiates the two.
Trap 7
"Abetalipoproteinemia causes high triglycerides and high cholesterol because fat isn't absorbed."
WRONG. Abetalipoproteinemia → absent chylomicrons → FAT AND VITAMIN MALABSORPTION → LOW serum lipids (not high). Steatorrhea (fatty stools). Hypocholesterolemia (not hypercholesterolemia). Confused students think "fat can't be packaged = high circulating fat," but actually fat never enters the blood at all.
Trap 8
"Intrinsic factor deficiency is the only cause of B12 malabsorption."
WRONG. B12 absorption requires: (1) IF from parietal cells (pernicious anemia if deficient), (2) Terminal ileum intact (ileal Crohn's, ileal resection, tropical sprue), (3) Transcobalamin II in blood (rare genetic defect). You can have normal IF but still malabsorb B12 if terminal ileum is diseased. Ask: "Is it stomach or ileum?"
HY Reference Tables
SI Anatomy & Function
Structure
Location/Function
Clinical Pearl
Villi
Finger-like projections; lamina propria + epithelium; lacteals inside
Removed in villous atrophy (celiac, tropical sprue, whipple's)