Week 4 - Gallbladder & Pancreas Flashcards
Why does cholecystitis cause ipsilateral back, shoulder and scapular pain?
- Referred pain.
- Visceral afferents ~T7-T9 run with sympathetic efferents → epigastric, right shoulder and infra scapular regions → referred pain.
Outline disorders of the gallbladder and pancreas.
Disorders:
• 95% cholelithiasis (usually associated with cholecystitis - only occasionally without gallstones).
• 5% other:
- Choledocolithiasis, cholangitis.
- Biliary atresia (intra and extra) - congenital.
- Primary biliary cirrhosis and sclerosing cholangitis (intra).
- Secondary biliary cirrhosis (complication of other obstructions).
- Carcinoma gallbladder*
- Cholangiocarcinoma*
Pancreatic disorders:
• Congenital (pancreas divisum - most common), pancreatitis (acute and chronic).
• Neoplasms - carcinoma pancreas.
What is the difference between cholelithiasis and choledocolithiasis?
- Cholelithiasis - stones in gallbladder - symptoms caused by gallstone obstructing the neck of the gallbladder - commonest cause of acute cholecystitis - surgery to remove stones.
- Choledocholithiasis - one of the stones getting into the bile duct and obstructing.
- Mixed cholesterol gallstones most common.
Outline cholecystitis: • Risk factors. • Pathogenesis. • Types. • Complications.
• Inflammation of the gallbladder.
Risk factors:
• Gallstones (95%) - commonest cause (cholelithiasis).
• Female, fat, forty, fertile.
Pathogenesis:
• Obstruction → stasis → increased pressure → ischaemia → mucosal damage by bile salt (detergent) → inflammation, infection.
• Obstruction by small gallstone leading to stasis of the bile (concentration of bile) → increased pressure causing ischaemia and then mucosal damage caused by bile salt (detergent - like a soap - begins to digest gallbladder wall) → causes inflammation and secondary infections.
Types: • Acute. • Chronic. • Acute on chronic (most common). • Cholesterosis (rare).
Complications:
• Cholangitis (inflammation spreading onto biliary tree), secondary biliary cirrhosis.
• Empyema (pus in gallbladder), rupture, peritonitis.
Describe the aetiology and pathogenesis of acute cholecystitis.
Aetiology:
• 90% cholelithiasis.
• 10% acalculous - trauma, burns, sepsis (10% of cases can be without stones e.g. trauma, dehydration, burns, sepsis. Typically in an ICU patient).
• Female, fat, forty, fertile.
Pathogenesis:
• Neck obstruction by a small gallstone → stasis, increased pressure, ischaemia, mucosal damage by bile salt (detergent action) → inflammation → secondary infection (E. coli) → empyema (complication).
• All this occurs rapidly - acute.
Identify the clinical features and complications of acute cholecystitis.
Clinical features:
• Biliary pain (steady*, progressive RUQ to right shoulder). Severe & prolonged abdominal pain in right upper quadrant + epigastrium.
• Obstructive jaundice in 20% (CBD obstruction).
• Fever.
• Vomiting.
• Local peritonism.
• Murphy’s sign +ve.
Complications:
• Perforation, cholangitis, gangrene, gallstone ileus when stone enters GIT.
- Acute pain known as biliary colic but typically biliary pain is not colicky because of very thin muscular layer and almost absent muscularis mucosa (contractions not present). Steady, progressively increasing, radiates from RUQ to right shoulder, hypogastrium or to the back.
- The main difference from biliary colic is the inflammatory component (local peritonism, fever, increased WCC).
- Obstructive jaundice when a stone totally obstructs the common bile duct. If the stone moves to the CBD, obstructive jaundice or cholangitis may occur.
- Complications - cholangitis, empyema, gangrene, rupture, perforation, gallstone ileus, mucocoele, pancreatitis, peritonitis, carcinoma.
Describe the morphology of acute cholecystitis.
- Acute inflammation (severe oedema), vasodilation, haemorrhage, plenty of neutrophils.
- May lead to gangrene or pus formation (empyema).
- Enlarged gallbladder with thickened wall.
- Mucosal oedema.
- Bright red/blotchy to green-black colour.
- Necrosis/gangrene (due ischaemia).
- Haemorrhage, pus.
- Presence of gallstone.
Identify the investigations for acute cholecystitis.
- Increased WBC.
- Serum amylase normal (increased in pancreatitis - suspect if amylase increased).
- LFTs - mild jaundice in 20% - obstructive.
- Ultrasound shows gallbladder thickening and gallstones but CT is clearer. Thick walled, shrunken gallbladder, pericholecystic fluid, stones, CBD (dilated if >6mm).
Outline chronic cholecystitis.
- Recurrent acute or mild, chronic biliary pain (some obstruction, gradually released by movement of stones).
- Obstruction or continuous irritation by the stones causing chronic inflammation.
- Typically present with nausea, vomiting, intolerance for fatty food. Flatulent dyspepsia - vague abdominal discomfort, distension, nausea, flatulence and fat intolerance.
- Same aetiology and pathogenesis as acute cholecystitis, FFFF - only difference with chronic is mild thickening of the gallbladder and thick bile (bile becomes very concentrated - known as biliary gravel).
- Thick bile - biliary gravel.
Microscopy:
• Chronic inflammation (inflammatory cells - lymphocytes), thick fibrotic wall (fibrosis).
• Hypertrophy of muscle, fibrosis and atrophy of mucosal gland.
• Aschoff-Rokitansky sinuses - excess luminal pressure pushes glands through muscular layer.
- Increased pressure causes herniation of the mucosa into the muscle layer - known as Aschoff Rokitansky sinuses - herniation of one of the mucosal glands through the mucosa - it is seen in chronic inflammation.
Outline acalculous cholecystitis.
• Cholecystitis without gallstones - usually seen in patients with sepsis, hypotension, trauma, burns, diabetes etc.
• Secondary to ischaemia → decreased movement - stasis.
- Usually secondary to ischaemia of the wall resulting in decreased protection - damage by the bile. Decreased movement resulting in stasis of the bile → all this causes bile concentration known as bile sludge → causes obstruction without stone.
• Biliary sludge - obstruction without stone.
• Mild biliary symptoms (primary disease is prominent) - primary disease such as sepsis, hypotension, trauma, burns usually take over the clinical features.
• High rate of gangrene or perforation - common - importance of knowing and investigating for cholecystitis.
What is cholesterolosis?
- Strawberry gallbladder - asymptomatic/chronic cholecystitis.
- Peculiar type of chronic cholecystitis where excess cholesterol gets accumulated within the folds of the mucosa causing multiple (hundreds) small polyps.
- Foamy macrophages (containing cholesterol) within the mucosal folds.
- Known as strawberry gallbladder because of the appearance - yellow nodes.
- Due to minute polyps - cholesterolosis.
- Characterised by deposits of cholesterol in tissue (excess cholesterol in mucosal folds).
- Is clinically not significant but may present as chronic cholecystitis.
- Condition resulting from disturbance in lipid metabolism.
Outline cholelithiasis:
• Epidemiology.
• Risk factors.
• Types.
• Stones in the biliary tree.
• Gallstones - 95% of gallbladder disorders (5-10% acalculus cholecystitis - non gallstone).
• Incidence - West 20-40%, Asian 2-4% (common in Western Caucasians (20-40% of population), less common in Asians).
• FFFF* - pneumonic to remember the risk factors for development of cholelithiasis. But also oral contraceptives (oestrogen), disorders of metabolism and hyperlipidaemias (congenital/familial) - leads to excess cholesterol or low motility leading to stasis of bile. Also pregnancy, diabetes (patients have increased cholesterol).
• 70-80% asymptomatic - 4%/year - symptomatic*
- Asymptomatic - have stones but they don’t know. 4% of these will start to develop symptoms at some time during their life.
2 major types:
• 80% - mixed cholesterol stones with calcium, bile, blood. Most common - predominant cholesterol with other components such as bile, bile pigments, cells, blood, calcium.
• 20% - pigment stones - black (haemoglobin - Asians), brown (calcium - infection, IBD), yellow (pure cholesterol).
- Pigment stones - dark black due to haemoglobin - common in Asians, due to haemolytic anaemia. Asians and Africans - patients with haemolytic anaemia due to bilirubin. Can occur in anyone. Brown stones rare - predominanty calcium, secondary to infection, IBD, CF. Yellow - pure round cholesterol stones (spikes on surface, typically causes bleeding - suspect severe hypercholesterolaemia).
Outline the aetiology and pathogenesis of cholelithiasis.
- Crystallisation of bile (cholesterol).
- Bile: cholesterol, bile salts and bile pigment. Cholesterol is made soluble by bile salts and lecithins (detergents - keep cholesterol in solution). If the concentrations vary, different stones may form.
4 aetiologic factors:
• Age and sex: female, fair, fat, forty, fertile - more susceptible but can occur in anyone.
• Environmental: increased estrogen, OCD (oral contraceptive drugs), pregnancy, diabetes, obesity, rapid weight loss (rapid weight loss therapy - too much cholesterol - can form stones).
• Acquired: bile stasis, secondary infections, haemolysis.
• Hereditary: ABCG8 gene mutation - sterol transporter - causes excess cholesterol within bile. *EXAM HINT.
- 4 pathogenic factors: increased cholesterol/decreased bile salts, stasis, reflux and infection.
- 4 factors cause deposition of cholesterol crystals → stone formation. Whatever causes increased cholesterol or decreased bile salts leads to build up of cholesterol. Stasis of bile, pancreatic enzyme reflux into gallbladder, infections.
- When there is crystallization or stasis → gallbladder becomes inflamed → deposition of cholesterol → forms stones → one of the small stones obstructs → leads to acute inflammation.
- Normally, bile secreted and collected in gallbladder. With fat food → stimulation of CCK → contracts gallbladder releasing bile into CBD → then into duodenum. Approx. 1L/day.
Describe the clinical features of cholelithiasis.
• Triad - RUQ steady pain associated with fever and leukocytosis. Progressive, radiates to right shoulder/back - biliary colic*
- Known as biliary colic but pain is typically not colicky. Steady pain because gallbladder has less muscle → muscular spasm is not prominent. Inflammation causes constant, gradually increasing pain. However, most commonly asymptomatic.
• Chronic - fat intolerance, flatulence → clay stools.
- Commonest presentation - fat intolerance (upset stomach following fatty food) and flatulence leading to clay stools because of obstruction to bile flow (fat indigestion occurs, fat remains in stool).
- Clay stool - foul smelling, pale, sticks to toilet bowl - due to lack of bile.
Identify the laboratory investigations of cholelithiasis.
• Ultrasound.
• X-ray - only 20% of mixed cholesterol stones and brown (infective) stones are radio-opaque (generally not used).
• In 20% mild increase conjugated bilirubin, AST & ALT (<5 fold) due to CBD obstruction.
- Usually normal, no abnormality. Acute symptoms - increased leukocytosis (acute inflammation).
- In 20% of cases when a stone obstructs CBD - there is conjugated hyperbilirubinemia. AST and ALT mild to moderate increase.
Describe the morphology of mixed cholesterol stones.
- Commonest.
- Yellowish (golden) grey brown.
- Shiny faceted stones (faceted due to continuous rubbing).
- Varying colours based on contents.
- Composition - cholesterol >50% + bile + cells + blood + calcium (~10%).
- Usually radiolucent - not seen on X-ray. Only when calcium is greater than 10% - can be seen on X-ray.
- Bile becomes thick, dark and it stains - bile gravel (thick bile due to stasis or due to obstruction).
