cholelithiasis, cholecystitis, and pancreatitis Flashcards
gallbladder
- lies in the gallbladder fossa on the inferior surface of the right hepatic lobe
- 7-10cm long
- has a fundus, body and neck
- stores and concentrates bile produced by the liver
- bile released into the duodenum after ingestion of food - cholecystokinin
bile is produced by
the liver
hepatic bile contains
- water
- bile acids
- bile salts
- bilirubin
- cholesterol
- phospholipids
- excreted hormones and drugs
function of bile
aid in the digestion of fats including fat soluble vitamins
excretion of bilirubin, excess cholesterol, xenobiotics and trace metals
bile acids
catabolic products and cholesterol, act to soubise cholesterol
bile salts formed by
formed by the conjugation of bile acids with taurine or glycine
bilirubin is
the end product of haem degradation
cholelithiasis means
gallstones
cholelithiasis summary
- common
- 20% will develop biliary colic (pain associated with cholesterol)
types of gall stones
cholesterol - >50% crystalline cholesterol monohydrate
pigment - (black or brown) - bilirubin calcium salts
pathogenesis of cholesterol stones
bile salts and phospholipids render cholesterol soluble in bile
when bile cholesterol concentration exceed the solubising capacity of bile (supersaturation) cholesterol nucleates into solid cholesterol monohydrate crystals
four conditions contribute to cholesterol GS formation
- supersaturation
- hypo mobility of GB
- cholesterol nucleation
- hyper secretion of mucous traps nucleated crystals leading to aggregation - biliary sludge
black stones
disorders that lead to elevated levels of unconjugated bilirubin in bile egg haemolytic syndromes, severe ileal dysfunction predispose to pigment stoma formation (unconjugated bilirubin combines with calcium to form calcium bilirubinate
brown stones
tend to form in bile ducts, contain bacterial degradation products of biliary lipids, calcium salts of fatty acids, unconjugated bilirubin and precipitated cholesterol
appearance of cholesterol stones
yellow, small or large, single or multiple
appearance of black stones
small, black, firm, multiple
appearance of brown stones
large, brown, soft, single or few>multiple
associated conditions of cholesterol stones
usually one
genetic/environmental factors
associated conditions of black stones
haemolysis, alcoholism, chrons disease, cirrhosis
associated conditions of brown stones
biliary infections
clinical presentation of gallstones
80% asymptomatic
biliary colic/cholecystitis/complications
complications of gall stones
empyema perforation fistula cholangitis obstructive cholestasis pancreatitis gallstone ileus increased risk of carcinoma
cholecystitis
may be acute or chronic
gall stones result in the inflammation of the gall bladder
calculous - due to a stone
acalculous - a stone can’t be found
acute calculous cholecystitis
right upper quadrant pain, fever, leukocytosis associated with gallbladder inflammation
in the majority of patients, acute cholecystitis is caused by gallstone obstruction of neck or cystic duct
obstruction
chemical irritation
mechanical irritation
ischaemia
superimposed infection eg. e coli, enterococcus, klebsiella, and enterobacter
what is released in response to gallbladder inflammation
inflammatory mediators which further propagate inflammation
chemical irritation
lysolecithin - produced from lecithin, a normal constituent of bile
this enzyme may be released into the gallbladder following trauma to the gallbladder wall from an impacted gallstone
acute acalculous cholecystitis develops in
5-10% of patients that udergo cholecystectomy
associated conditions in acute acalculous cholecystitis
trauma, non-biliary surgery, sepsis, bruins, parenteral nutrition, mechanical ventilation, multiple blood transfusions, prior uses of narcotics or AB
mechanisms of acute acalculous CS
bile stasis and increased viscosity resulting in obstruction, mucosal ischaemia, infection, external obstruction of biliary tree
clinical symptoms of acute acalculous CS
smilar to calculous but may be insidious and masked by the precipitating/associated conditions
incidence of gangrene and perforation is higher
clinical presentation of of cholecystitis
biliary pain - RUQ/epigastrium constant, severe, radiate to back or shoulder fever nausea and vomiting murphy's sign guarding resistance of symptoms beyond 24hours leukocytosis hyperbilirubinaemia - obstruction of CBD
investigations of cholecystitis
bloods
chest x ray to rule out other cause
ultrasound the gall bladder to check for thinkening of the gall bladder wall or fluid around
CT scan
histology of cholecystitis
mucosal damage - ulceration inflammation - acute/chronic mucosal regeneration with hyperplasia fibrosis (repair) muscle hypertrophy diverticula
treatment of cholecystitis
observe vital signs, pain relief
surgery - more often after the acute attack has settled, should be 2-3 days after onset of symptoms
can be open or laparoscopic operation
why should surgery be done 2-3 days after onset of symptoms
after this period, development off adhesions and transmural inflammation increases risk of complications
chronic cholecystitis
90% calculous
may be identified after repeated bouts of acute cholecystitis
most common symptoms is episodic abdominal pain in epigastrium or RUQ, can be precipitated by food
mild of moderate tenderness on palpation of the gallbladder
predominantly mononuclear inflammatory infiltrate in the LP with or without extension into the muscularis and pericholecystic tissues
fibrosis
metaplastic changes
mechanism of chronic cholecystitis
similar to acute cholecystitis
supersaturation of bile leading to chronic inflammation and stone formation
macroscopic findings in chronic cholecystitis
serosa may be dulled, fibrous adhesions, churned and fibrotic, wall this or thick, attenuated and trabeculated muscosa
pancreas
outpouching of the duodenum, formed by fusion of ventral and dorsal bud; fusion of ventral and distal portion of the dorsal duct form the MPD, the proximal portion of the dorsal duct can persist to form the accessory duct of Santorini
parts of the pancreas
head, uncinate, neck, body and tail
two histological components of the pancreas
endocrine and exocrine
pancreas divism
most common congenital anomaly - incidence 3-10%
remnant of Santorini (minor duct) is not connected to the main pancreatic duct
most of the pancreas is being drained by the small duct of Santorini
leads to pancreatitis in many patients
acute pancreatitis
reversible pancreatic injury associated with inflammation
common
aetiological factors of acute pancreatitis
- genetic - mutations in cationic trypsinogen and trypsin inhibitor genes, or CF transmembrane conductance regulator gene
- metabolic - hyperlipoproteinaemia, hypercalcaemia, drugs
- mechanical - pancreatic tumours, trauma, iatrogenic, pancreatic divest, parasites
- vascular - shock, atheroembolism, vasculitis
infectious - mumps
mechanism of pancreatitis
pancreatic duct obstruction
primary acing cell injury
defective intracellular transport of proenzymes within acing cells
end result its auto digestion of pancreas by inappropriately released and activated pancreatic enzymes (trypsin key enzyme, as it can activate other proenzymes, the kinin system, clotting and complement systems)
consequences of pancreatitis
fat necrosis, interstitial inflammation, vascular damage and haemorrhage, parenchymal necrosis
fat necrosis
release of fatty acids, which bind calcium and magnesium ions to form insoluble soaps (fat saponification)
clinical presentation of pancreatitis
20% severe
severe cases - shock with multi organ failure due to release of toxic enzymes, cytokines and the inflammatory mediators into circulation
diagnosis of acute pancreatitis
2 of these 3 features needed
- abdominal pain consistent with acute pancreatitis - acute onset, persistent, severe, epigastric pain often radiating to back
- serum lipase/amylase at least 3 times greater than upper limit of normal
- characteristic finding on ultrasound, CT or less commonly MRI
investigations for acute pancreatitis
- biochemical - amylase and lipase, leukocytosis for gall stones, LFTs
- UC
- CT - diagnostic uncertainty after US, severe cases, failure to improve or deterioration, complication
- ERCP - endoscopic, asses whether gallstones are present and retrieve gallstones
- management - nil by mouth, supportive, relieve obstructions, manage complications
local complications of acute pancreatitis
- peripancreatic fluid collection
- pseudocyst
- necrotic collection
- gastric outlet dysfunction
- splenic and portal vein thrombosis
systemic complications of acute pancreatitis
- exacerbation of pre-existing co morbidity
- organ failure
chronic pancreatitis
fibroinflammatory disorder in which acing compartment is replaced by fibrosis leading to exocrine insufficiency and in the late stages destruction of endocrine parenchyma
same aetiology at AP
clinical presentation of chronic pancreatitis
- recurrent episodes of AP
- constant pain - epigastric radiates to the back and can be partially relieved by sitting up and leaning forward
- symptoms related to local complications eg. pseudocyst, carcinoma
- endocrine or exocrine insufficiency
hereditary pancreatitis
characteristically
- recurrent bouts of pancreatitis beginning in childhood
- gremlin mutation neither result in enhances activation of trypsin or inhibit/impede its inactivation
autoimmune pancreatitis
mass forming inflammatory lesion of the pancreas - may mimic cancer
other times, is a diffuse radiological/macroscopic abnormality of pancreas identified
two clinicopathological subtypes of autoimmune apocreatitis
- type 1 - IgG4 related disease
- type 2 - not IgG4 related, usually associated with IBD
treatment for autoimmune pancreatitis
steroids
aetiology of autoimmune pancreatitis
multifactorial - genetic factors, bacterial infection, autoimmunity
