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pathology 2 > cholelithiasis, cholecystitis, and pancreatitis > Flashcards

cholelithiasis, cholecystitis, and pancreatitis Flashcards

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1
Q

gallbladder

A
  • 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
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2
Q

bile is produced by

A

the liver

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3
Q

hepatic bile contains

A
  • water
  • bile acids
  • bile salts
  • bilirubin
  • cholesterol
  • phospholipids
  • excreted hormones and drugs
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4
Q

function of bile

A

aid in the digestion of fats including fat soluble vitamins

excretion of bilirubin, excess cholesterol, xenobiotics and trace metals

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5
Q

bile acids

A

catabolic products and cholesterol, act to soubise cholesterol

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6
Q

bile salts formed by

A

formed by the conjugation of bile acids with taurine or glycine

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7
Q

bilirubin is

A

the end product of haem degradation

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8
Q

cholelithiasis means

A

gallstones

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9
Q

cholelithiasis summary

A
  • common

- 20% will develop biliary colic (pain associated with cholesterol)

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10
Q

types of gall stones

A

cholesterol - >50% crystalline cholesterol monohydrate

pigment - (black or brown) - bilirubin calcium salts

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11
Q

pathogenesis of cholesterol stones

A

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

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12
Q

four conditions contribute to cholesterol GS formation

A
  • supersaturation
  • hypo mobility of GB
  • cholesterol nucleation
  • hyper secretion of mucous traps nucleated crystals leading to aggregation - biliary sludge
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13
Q

black stones

A

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

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14
Q

brown stones

A

tend to form in bile ducts, contain bacterial degradation products of biliary lipids, calcium salts of fatty acids, unconjugated bilirubin and precipitated cholesterol

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15
Q

appearance of cholesterol stones

A

yellow, small or large, single or multiple

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16
Q

appearance of black stones

A

small, black, firm, multiple

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17
Q

appearance of brown stones

A

large, brown, soft, single or few>multiple

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18
Q

associated conditions of cholesterol stones

A

usually one

genetic/environmental factors

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19
Q

associated conditions of black stones

A

haemolysis, alcoholism, chrons disease, cirrhosis

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20
Q

associated conditions of brown stones

A

biliary infections

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21
Q

clinical presentation of gallstones

A

80% asymptomatic

biliary colic/cholecystitis/complications

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22
Q

complications of gall stones

A 
empyema
perforation 
fistula 
cholangitis 
obstructive cholestasis 
pancreatitis 
gallstone ileus 
increased risk of carcinoma
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23
Q

cholecystitis

A

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

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24
Q

acute calculous cholecystitis

A

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

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25
obstruction
chemical irritation mechanical irritation ischaemia superimposed infection eg. e coli, enterococcus, klebsiella, and enterobacter
26
what is released in response to gallbladder inflammation
inflammatory mediators which further propagate inflammation
27
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
28
acute acalculous cholecystitis develops in
5-10% of patients that udergo cholecystectomy
29
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
30
mechanisms of acute acalculous CS
bile stasis and increased viscosity resulting in obstruction, mucosal ischaemia, infection, external obstruction of biliary tree
31
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
32
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 ```
33
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
34
histology of cholecystitis
``` mucosal damage - ulceration inflammation - acute/chronic mucosal regeneration with hyperplasia fibrosis (repair) muscle hypertrophy diverticula ```
35
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
36
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
37
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
38
mechanism of chronic cholecystitis
similar to acute cholecystitis | supersaturation of bile leading to chronic inflammation and stone formation
39
macroscopic findings in chronic cholecystitis
serosa may be dulled, fibrous adhesions, churned and fibrotic, wall this or thick, attenuated and trabeculated muscosa
40
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
41
parts of the pancreas
head, uncinate, neck, body and tail
42
two histological components of the pancreas
endocrine and exocrine
43
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
44
acute pancreatitis
reversible pancreatic injury associated with inflammation | common
45
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
46
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)
47
consequences of pancreatitis
fat necrosis, interstitial inflammation, vascular damage and haemorrhage, parenchymal necrosis
48
fat necrosis
release of fatty acids, which bind calcium and magnesium ions to form insoluble soaps (fat saponification)
49
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
50
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
51
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
52
local complications of acute pancreatitis
- peripancreatic fluid collection - pseudocyst - necrotic collection - gastric outlet dysfunction - splenic and portal vein thrombosis
53
systemic complications of acute pancreatitis
- exacerbation of pre-existing co morbidity | - organ failure
54
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
55
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
56
hereditary pancreatitis
characteristically - recurrent bouts of pancreatitis beginning in childhood - gremlin mutation neither result in enhances activation of trypsin or inhibit/impede its inactivation
57
autoimmune pancreatitis
mass forming inflammatory lesion of the pancreas - may mimic cancer other times, is a diffuse radiological/macroscopic abnormality of pancreas identified
58
two clinicopathological subtypes of autoimmune apocreatitis
- type 1 - IgG4 related disease | - type 2 - not IgG4 related, usually associated with IBD
59
treatment for autoimmune pancreatitis
steroids
60
aetiology of autoimmune pancreatitis
multifactorial - genetic factors, bacterial infection, autoimmunity

pathology 2 (47 decks)

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