Cholelithiasis
Cholelithiasis (Gallstones)
Overview
Formed from bile constituents: cholesterol, bile pigments, calcium salts + organic components. Usually gallbladder; sometimes extrahepatic ducts; rarely intrahepatic.
Risk factors — “4 F’s” (fat, female, fertile, forty) — mainly CHOLESTEROL stones
- Geography — Western world high, American Indians HIGHEST, Black Africans/Eastern world LOW
- Genetic — ↑1st-degree relative frequency, ↑cholesterol secretion despite normal intake. CYP7A1 mutation→↓cholesterol 7α-hydroxylase→↓bile acid synthesis→hypercholesterolaemia+stones
- Age — ↑with age (↑biliary cholesterol), rises after 40, presents 50s-60s
- Sex — 2x women (US: 20% women vs 8% men >40). ↑multiparous > nulliparous
- Drugs — oestrogen/OCPs (↑lithogenic bile via cholestatic effect), clofibrate
- Obesity — ↑cholesterol synthesis+excretion
- Diet — ↓fibre=↑risk; moderate ALCOHOL=protective
- GI disease — Crohn’s, ileal resection/bypass (interrupted enterohepatic circulation)
- PIGMENT stones specifically — haemolytic anaemia (↑unconjugated bilirubin), cirrhosis/hepatocellular disease — DIFFERENT risk profile from 4F’s, common confusion point
Pathogenesis
Cholesterol/mixed/sludge: cholesterol insoluble→normally solubilised as bilayered vesicles→mixed micelles(+bile acids). Excess cholesterol→unstable vesicles→crystals. 3 mechanisms:
- SUPERSATURATION — major initiator. ↑HMG-CoA reductase→↑cholesterol secretion. Contributing: ↓bile acid pool, ↑cholic→deoxycholic conversion. MDR3 mutation→↓phospholipid secretion→supersaturation. NECESSARY BUT NOT SUFFICIENT alone
- NUCLEATION — cholesterol monohydrate crystals. Pro-nucleating(mucin/non-mucin glycoproteins) vs anti-nucleating(apo AI/AII) balance. Occurs in mucin gel layer
- HYPOMOTILITY — normally CCK-driven emptying clears sludge. ↓CCK receptors→stasis→lithogenesis. Also explains post-lithotripsy recurrence
Pigment stones: chronic haemolysis(↑unconjugated bilirubin), alcoholic cirrhosis, chronic biliary infection(Clonorchis sinensis, Ascaris lumbricoides), demographic/genetic(rural, Asian).
Types (pure10% : mixed80% : combined10%)
Pure=usually NO inflammation. Mixed/combined=INVARIABLY chronic cholecystitis. Calcium=radio-opaque; cholesterol=radiolucent.
1. PURE (~10%):
- Cholesterol — solitary, oval, LARGE(≥3cm), hard smooth whitish-yellow, radiating crystals on cut section. →CHOLESTEROLOSIS(asymptomatic, mucosal macrophage deposits). Radiolucent(10-20% have Ca→opaque)
- Pigment — <20% cholesterol, multiple, JET-BLACK, small(<1cm), mulberry surface, soft/crushable. Gallbladder uninvolved
- Calcium carbonate — rare, multiple, grey-white, small, faceted, hard. No wall change
2. MIXED (80%, COMMONEST) — >50% cholesterol+Ca salts+bile pigments+fatty acids. Always multiple, multifaceted, sand-grain to ≥1cm. LAMINATED cut section (alternating layers=different deposition times). INVARIABLY chronic cholecystitis.
3. COMBINED (~10%) — solitary, large, smooth. Pure-stone nucleus+mixed shell (or reverse). Also chronic cholecystitis.
Clinical/complications
~50% ASYMPTOMATIC (“silent gallstones”) — debated management (surgeons: cholecystectomy; physicians: watchful waiting). Only ~10% of silent cases eventually symptomatic = evidence base for watchful waiting.
Complications:
- CHOLECYSTITIS — biliary colic(fatty meal), N/V, fever, leucocytosis, ↑bilirubin. Causal direction with stones uncertain
- CHOLEDOCHOLITHIASIS — stone passage/formation in ducts→pain+obstructive jaundice, ±ascending cholangitis fever
- MUCOCELE/EMPYEMA — mucocele=distension by mucinous secretion(impacted neck stone)→infection→empyema
- Biliary fistula — uncommon, biliary-bowel or gallbladder-skin
- Gallstone ileus — usually passes silently, occasionally→obstruction
- Pancreatitis — obstructive cholelithiasis→acute pancreatitis
- Gallbladder cancer — small doubtful risk increase
Clinical relevance
4F’s mnemonic = CHOLESTEROL stones specifically, NOT pigment stones (which follow haemolysis/cirrhosis/parasitic profile) — common mixing-up error. Supersaturation necessary-BUT-NOT-sufficient = key concept tying 3 mechanisms together (many have supersaturated bile without stones — nucleation+stasis are the extra required steps). Stone-type↔cholecystitis pattern (pure=usually clean; mixed/combined=invariably inflamed) = useful specimen-interpretation correlation. “~10% of silent stones become symptomatic” = specific evidence against reflexive cholecystectomy.
Cholelithiasis (Gallstones)
Overview
Formed from bile constituents: cholesterol, bile pigments, calcium salts + organic components. Usually gallbladder; sometimes extrahepatic ducts; rarely intrahepatic.
Risk factors — “4 F’s” (fat, female, fertile, forty) — mainly CHOLESTEROL stones
- Geography — Western world high, American Indians HIGHEST, Black Africans/Eastern world LOW
- Genetic — ↑1st-degree relative frequency, ↑cholesterol secretion despite normal intake. CYP7A1 mutation→↓cholesterol 7α-hydroxylase→↓bile acid synthesis→hypercholesterolaemia+stones
- Age — ↑with age (↑biliary cholesterol), rises after 40, presents 50s-60s
- Sex — 2x women (US: 20% women vs 8% men >40). ↑multiparous > nulliparous
- Drugs — oestrogen/OCPs (↑lithogenic bile via cholestatic effect), clofibrate
- Obesity — ↑cholesterol synthesis+excretion
- Diet — ↓fibre=↑risk; moderate ALCOHOL=protective
- GI disease — Crohn’s, ileal resection/bypass (interrupted enterohepatic circulation)
- PIGMENT stones specifically — haemolytic anaemia (↑unconjugated bilirubin), cirrhosis/hepatocellular disease — DIFFERENT risk profile from 4F’s, common confusion point
Pathogenesis
Cholesterol/mixed/sludge: cholesterol insoluble→normally solubilised as bilayered vesicles→mixed micelles(+bile acids). Excess cholesterol→unstable vesicles→crystals. 3 mechanisms:
- SUPERSATURATION — major initiator. ↑HMG-CoA reductase→↑cholesterol secretion. Contributing: ↓bile acid pool, ↑cholic→deoxycholic conversion. MDR3 mutation→↓phospholipid secretion→supersaturation. NECESSARY BUT NOT SUFFICIENT alone
- NUCLEATION — cholesterol monohydrate crystals. Pro-nucleating(mucin/non-mucin glycoproteins) vs anti-nucleating(apo AI/AII) balance. Occurs in mucin gel layer
- HYPOMOTILITY — normally CCK-driven emptying clears sludge. ↓CCK receptors→stasis→lithogenesis. Also explains post-lithotripsy recurrence
Pigment stones: chronic haemolysis(↑unconjugated bilirubin), alcoholic cirrhosis, chronic biliary infection(Clonorchis sinensis, Ascaris lumbricoides), demographic/genetic(rural, Asian).
Types (pure10% : mixed80% : combined10%)
Pure=usually NO inflammation. Mixed/combined=INVARIABLY chronic cholecystitis. Calcium=radio-opaque; cholesterol=radiolucent.
1. PURE (~10%):
- Cholesterol — solitary, oval, LARGE(≥3cm), hard smooth whitish-yellow, radiating crystals on cut section. →CHOLESTEROLOSIS(asymptomatic, mucosal macrophage deposits). Radiolucent(10-20% have Ca→opaque)
- Pigment — <20% cholesterol, multiple, JET-BLACK, small(<1cm), mulberry surface, soft/crushable. Gallbladder uninvolved
- Calcium carbonate — rare, multiple, grey-white, small, faceted, hard. No wall change
2. MIXED (80%, COMMONEST) — >50% cholesterol+Ca salts+bile pigments+fatty acids. Always multiple, multifaceted, sand-grain to ≥1cm. LAMINATED cut section (alternating layers=different deposition times). INVARIABLY chronic cholecystitis.
3. COMBINED (~10%) — solitary, large, smooth. Pure-stone nucleus+mixed shell (or reverse). Also chronic cholecystitis.
Clinical/complications
~50% ASYMPTOMATIC (“silent gallstones”) — debated management (surgeons: cholecystectomy; physicians: watchful waiting). Only ~10% of silent cases eventually symptomatic = evidence base for watchful waiting.
Complications:
- CHOLECYSTITIS — biliary colic(fatty meal), N/V, fever, leucocytosis, ↑bilirubin. Causal direction with stones uncertain
- CHOLEDOCHOLITHIASIS — stone passage/formation in ducts→pain+obstructive jaundice, ±ascending cholangitis fever
- MUCOCELE/EMPYEMA — mucocele=distension by mucinous secretion(impacted neck stone)→infection→empyema
- Biliary fistula — uncommon, biliary-bowel or gallbladder-skin
- Gallstone ileus — usually passes silently, occasionally→obstruction
- Pancreatitis — obstructive cholelithiasis→acute pancreatitis
- Gallbladder cancer — small doubtful risk increase
Clinical relevance
4F’s mnemonic = CHOLESTEROL stones specifically, NOT pigment stones (which follow haemolysis/cirrhosis/parasitic profile) — common mixing-up error. Supersaturation necessary-BUT-NOT-sufficient = key concept tying 3 mechanisms together (many have supersaturated bile without stones — nucleation+stasis are the extra required steps). Stone-type↔cholecystitis pattern (pure=usually clean; mixed/combined=invariably inflamed) = useful specimen-interpretation correlation. “~10% of silent stones become symptomatic” = specific evidence against reflexive cholecystectomy.
Cholelithiasis (Gallstones)
Overview
Gallstones form from bile constituents — cholesterol, bile pigments, calcium salts — plus other organic components, in varying proportions. Usually form in the gallbladder, sometimes in extrahepatic biliary passages, rarely in larger intrahepatic ducts.
Risk Factors
Incidence varies by geography, age, gender, diet, and other factors — classically summarised by the “4 F’s”: fat, female, fertile (multipara), forty. (These largely apply to cholesterol stones.)
- Geography — prevalent through the Western world; American Indians have the highest known prevalence; Black Africans and Eastern-world populations are relatively spared.
- Genetic factors — increased frequency in first-degree relatives; gallstone patients secrete more dietary cholesterol into bile despite similar intake. CYP7A1 gene mutation → cholesterol 7α-hydroxylase deficiency (impairs bile acid synthesis) → hypercholesterolaemia and gallstones.
- Age — steadily rising prevalence with age (higher biliary cholesterol content); incidence rises after 40, typical presentation in 50s–60s.
- Sex — twice as frequent in women; US autopsy series: ~20% women vs 8% men over 40; higher in multiparous than nulliparous women.
- Drugs — oestrogen therapy/OCPs raise incidence (more lithogenic bile from oestrogen’s cholestatic effect); similarly, cholesterol-lowering drugs like clofibrate.
- Obesity — associated with increased cholesterol synthesis/excretion.
- Diet — low dietary fibre linked to higher prevalence; moderate alcohol consumption appears protective.
- GI diseases — Crohn’s disease, ileal resection/bypass — interrupt enterohepatic circulation, promoting gallstone formation.
- Pigment stone-specific factors — haemolytic anaemias (↑unconjugated bilirubin in bile), cirrhosis/hepatocellular disease, more frequent overall.
Pathogenesis
Cholesterol, Mixed Gallstones, and Biliary Sludge
Cholesterol is water-insoluble, normally solubilised by phospholipid (lecithin) as bilayered vesicles, converted to mixed micelles with bile acids as the third constituent. Excess cholesterol relative to the other two leaves unstable cholesterol-rich vesicles that aggregate into crystals. Three mechanisms:
- Supersaturation of bile — the major initiating mechanism: enhanced HMG-CoA reductase activity (regulating cholesterol synthesis/hepatic uptake) drives increased biliary cholesterol secretion. Contributing disturbances: reduced bile acid pool (rapid loss into intestine/colon); increased cholic-to-deoxycholic acid conversion (deoxycholate hypersecretion linked to cholesterol hypersecretion). MDR3 gene mutation impairs phospholipid secretion into bile → cholesterol supersaturation. Supersaturation is necessary but not sufficient alone for stone formation.
- Cholesterol nucleation — cholesterol monohydrate crystal nucleation, accelerated by pro-nucleating factors (mucin and non-mucin glycoproteins from gallbladder epithelium) or deficient anti-nucleating factors (apolipoproteins AI/AII, some glycoproteins); nucleation likely occurs in the gallbladder mucin gel layer, followed by continued crystal addition/precipitation.
- Gallbladder hypomotility — normally the gallbladder clears sludge/debris under cholecystokinin (CCK) stimulation; reduced CCK receptors impair emptying → biliary sludge stasis → lithogenesis. Emptying defects also contribute to stone recurrence after lithotripsy.
Pigment Gallstones
Driven by: chronic haemolysis (↑ unconjugated bilirubin in bile), alcoholic cirrhosis, chronic biliary tract infection (parasitic — Clonorchis sinensis, Ascaris lumbricoides), and demographic/genetic factors (rural settings, Asian prevalence).
Types of Gallstones
Three major types: pure, mixed, combined — mixed is commonest (80%), pure and combined 10% each. Pure-stone gallbladders show no significant inflammation; chronic cholecystitis is invariably present with mixed or combined stones. Calcium content renders stones radio-opaque; cholesterol stones are radiolucent.
1. Pure gallstones (~10%) — three sub-types:
- Pure cholesterol — usually solitary, oval, large (≥3 cm), hard smooth whitish-yellow glistening surface; cut section shows radiating glistening crystals. May deposit within gallbladder mucosal macrophages producing asymptomatic cholesterolosis. Radiolucent, but 10–20% contain calcium carbonate (radio-opaque).
- Pure pigment — mainly bile pigment/calcium bilirubinate, <20% cholesterol; multiple, jet-black, small (<1 cm), mulberry-like surface, soft/crushable; gallbladder usually uninvolved.
- Pure calcium carbonate — rare; multiple, grey-white, small (<1 cm), faceted, fairly hard; no gallbladder wall change.
2. Mixed gallstones (80%, commonest) — >50% cholesterol monohydrate plus calcium salts, bile pigments, fatty acids; always multiple, multifaceted (fit together), sand-grain to ≥1 cm; laminated cut section (alternating dark pigment/pale layers from different-time deposition). Invariably accompanied by chronic cholecystitis.
3. Combined gallstones (~10%) — usually solitary, large, smooth-surfaced; a pure-stone nucleus with a mixed-stone shell, or vice versa. Also associated with chronic cholecystitis.
Clinical Manifestations and Complications
~50% of gallstones are asymptomatic (“silent gallstones”), found incidentally. Management of asymptomatic cases is debated (surgeons favour cholecystectomy, physicians favour watchful waiting) — follow-up shows only ~10% eventually become symptomatic. Symptomatic disease appears once complications develop:
- Cholecystitis — the gallstone-cholecystitis relationship is well-established though the causal direction is uncertain; symptoms include biliary colic (precipitated by fatty meals), nausea, vomiting, fever, leucocytosis, elevated serum bilirubin.
- Choledocholithiasis — stones passing into extrahepatic ducts/small bowel, or forming there directly; common bile duct stones cause pain and obstructive jaundice; fever from ascending bacterial cholangitis.
- Mucocele and empyema — mucocele (hydrops) = gallbladder distension by clear watery mucinous secretion from a stone impacted at the neck; infection converts this to empyema.
- Biliary fistula — uncommon; between biliary system and bowel, rarely gallbladder-to-skin.
- Gallstone ileus — most intestinal stones pass silently in faeces, but occasionally cause intestinal obstruction.
- Pancreatitis — obstructive cholelithiasis may precipitate acute pancreatitis.
- Gallbladder cancer — small, doubtful increased risk with cholelithiasis.
Clinical Relevance
- The 4 F’s mnemonic (fat, female, fertile, forty) is worth anchoring specifically to cholesterol stones — pigment stones follow a genuinely different risk profile (haemolysis, cirrhosis, parasitic infection) and applying the same mnemonic there is a common error.
- Supersaturation being necessary-but-not-sufficient for lithogenesis is the key conceptual point tying together the three mechanisms (supersaturation, nucleation, hypomotility) — many people have supersaturated bile without ever forming stones, because nucleation and stasis are the additional required steps.
- The stone-type-to-cholecystitis-association pattern (pure stones = usually no inflammation; mixed/combined = invariably chronic cholecystitis) is a useful diagnostic correlation when interpreting a cholecystectomy specimen.
- The “only ~10% of silent gallstones become symptomatic” statistic is the clinical evidence base behind the watchful-waiting argument for asymptomatic cholelithiasis, and is worth remembering as a specific counter to reflexive cholecystectomy.
Cholelithiasis (Gallstones)
Overview
Gallstones form from bile constituents — cholesterol, bile pigments, calcium salts — plus other organic components, in varying proportions. Usually form in the gallbladder, sometimes in extrahepatic biliary passages, rarely in larger intrahepatic ducts.
Risk Factors
Incidence varies by geography, age, gender, diet, and other factors — classically summarised by the “4 F’s”: fat, female, fertile (multipara), forty. (These largely apply to cholesterol stones.)
- Geography — prevalent through the Western world; American Indians have the highest known prevalence; Black Africans and Eastern-world populations are relatively spared.
- Genetic factors — increased frequency in first-degree relatives; gallstone patients secrete more dietary cholesterol into bile despite similar intake. CYP7A1 gene mutation → cholesterol 7α-hydroxylase deficiency (impairs bile acid synthesis) → hypercholesterolaemia and gallstones.
- Age — steadily rising prevalence with age (higher biliary cholesterol content); incidence rises after 40, typical presentation in 50s–60s.
- Sex — twice as frequent in women; US autopsy series: ~20% women vs 8% men over 40; higher in multiparous than nulliparous women.
- Drugs — oestrogen therapy/OCPs raise incidence (more lithogenic bile from oestrogen’s cholestatic effect); similarly, cholesterol-lowering drugs like clofibrate.
- Obesity — associated with increased cholesterol synthesis/excretion.
- Diet — low dietary fibre linked to higher prevalence; moderate alcohol consumption appears protective.
- GI diseases — Crohn’s disease, ileal resection/bypass — interrupt enterohepatic circulation, promoting gallstone formation.
- Pigment stone-specific factors — haemolytic anaemias (↑unconjugated bilirubin in bile), cirrhosis/hepatocellular disease, more frequent overall.
Pathogenesis
Cholesterol, Mixed Gallstones, and Biliary Sludge
Cholesterol is water-insoluble, normally solubilised by phospholipid (lecithin) as bilayered vesicles, converted to mixed micelles with bile acids as the third constituent. Excess cholesterol relative to the other two leaves unstable cholesterol-rich vesicles that aggregate into crystals. Three mechanisms:
- Supersaturation of bile — the major initiating mechanism: enhanced HMG-CoA reductase activity (regulating cholesterol synthesis/hepatic uptake) drives increased biliary cholesterol secretion. Contributing disturbances: reduced bile acid pool (rapid loss into intestine/colon); increased cholic-to-deoxycholic acid conversion (deoxycholate hypersecretion linked to cholesterol hypersecretion). MDR3 gene mutation impairs phospholipid secretion into bile → cholesterol supersaturation. Supersaturation is necessary but not sufficient alone for stone formation.
- Cholesterol nucleation — cholesterol monohydrate crystal nucleation, accelerated by pro-nucleating factors (mucin and non-mucin glycoproteins from gallbladder epithelium) or deficient anti-nucleating factors (apolipoproteins AI/AII, some glycoproteins); nucleation likely occurs in the gallbladder mucin gel layer, followed by continued crystal addition/precipitation.
- Gallbladder hypomotility — normally the gallbladder clears sludge/debris under cholecystokinin (CCK) stimulation; reduced CCK receptors impair emptying → biliary sludge stasis → lithogenesis. Emptying defects also contribute to stone recurrence after lithotripsy.
Pigment Gallstones
Driven by: chronic haemolysis (↑ unconjugated bilirubin in bile), alcoholic cirrhosis, chronic biliary tract infection (parasitic — Clonorchis sinensis, Ascaris lumbricoides), and demographic/genetic factors (rural settings, Asian prevalence).
Types of Gallstones
Three major types: pure, mixed, combined — mixed is commonest (80%), pure and combined 10% each. Pure-stone gallbladders show no significant inflammation; chronic cholecystitis is invariably present with mixed or combined stones. Calcium content renders stones radio-opaque; cholesterol stones are radiolucent.
1. Pure gallstones (~10%) — three sub-types:
- Pure cholesterol — usually solitary, oval, large (≥3 cm), hard smooth whitish-yellow glistening surface; cut section shows radiating glistening crystals. May deposit within gallbladder mucosal macrophages producing asymptomatic cholesterolosis. Radiolucent, but 10–20% contain calcium carbonate (radio-opaque).
- Pure pigment — mainly bile pigment/calcium bilirubinate, <20% cholesterol; multiple, jet-black, small (<1 cm), mulberry-like surface, soft/crushable; gallbladder usually uninvolved.
- Pure calcium carbonate — rare; multiple, grey-white, small (<1 cm), faceted, fairly hard; no gallbladder wall change.
2. Mixed gallstones (80%, commonest) — >50% cholesterol monohydrate plus calcium salts, bile pigments, fatty acids; always multiple, multifaceted (fit together), sand-grain to ≥1 cm; laminated cut section (alternating dark pigment/pale layers from different-time deposition). Invariably accompanied by chronic cholecystitis.
3. Combined gallstones (~10%) — usually solitary, large, smooth-surfaced; a pure-stone nucleus with a mixed-stone shell, or vice versa. Also associated with chronic cholecystitis.
Clinical Manifestations and Complications
~50% of gallstones are asymptomatic (“silent gallstones”), found incidentally. Management of asymptomatic cases is debated (surgeons favour cholecystectomy, physicians favour watchful waiting) — follow-up shows only ~10% eventually become symptomatic. Symptomatic disease appears once complications develop:
- Cholecystitis — the gallstone-cholecystitis relationship is well-established though the causal direction is uncertain; symptoms include biliary colic (precipitated by fatty meals), nausea, vomiting, fever, leucocytosis, elevated serum bilirubin.
- Choledocholithiasis — stones passing into extrahepatic ducts/small bowel, or forming there directly; common bile duct stones cause pain and obstructive jaundice; fever from ascending bacterial cholangitis.
- Mucocele and empyema — mucocele (hydrops) = gallbladder distension by clear watery mucinous secretion from a stone impacted at the neck; infection converts this to empyema.
- Biliary fistula — uncommon; between biliary system and bowel, rarely gallbladder-to-skin.
- Gallstone ileus — most intestinal stones pass silently in faeces, but occasionally cause intestinal obstruction.
- Pancreatitis — obstructive cholelithiasis may precipitate acute pancreatitis.
- Gallbladder cancer — small, doubtful increased risk with cholelithiasis.
Clinical Relevance
- The 4 F’s mnemonic (fat, female, fertile, forty) is worth anchoring specifically to cholesterol stones — pigment stones follow a genuinely different risk profile (haemolysis, cirrhosis, parasitic infection) and applying the same mnemonic there is a common error.
- Supersaturation being necessary-but-not-sufficient for lithogenesis is the key conceptual point tying together the three mechanisms (supersaturation, nucleation, hypomotility) — many people have supersaturated bile without ever forming stones, because nucleation and stasis are the additional required steps.
- The stone-type-to-cholecystitis-association pattern (pure stones = usually no inflammation; mixed/combined = invariably chronic cholecystitis) is a useful diagnostic correlation when interpreting a cholecystectomy specimen.
- The “only ~10% of silent gallstones become symptomatic” statistic is the clinical evidence base behind the watchful-waiting argument for asymptomatic cholelithiasis, and is worth remembering as a specific counter to reflexive cholecystectomy.
Cholelithiasis (Gallstones)
- The three lithogenesis mechanisms (supersaturation → nucleation → hypomotility) as a sequential pathway with the necessary-but-not-sufficient point marked
- Pure/mixed/combined gallstone cross-sections side by side showing their distinct internal structure
Cholelithiasis (Gallstones)
- The three lithogenesis mechanisms (supersaturation → nucleation → hypomotility) as a sequential pathway with the necessary-but-not-sufficient point marked
- Pure/mixed/combined gallstone cross-sections side by side showing their distinct internal structure
Short Answers (2)
Multiple Choice Questions (2)
My Sticky Notes
Personal revision notes, mnemonics and reminders.
