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pathology 2 > cholelithiasis, cholecystitis, and pancreatitis > Flashcards

cholelithiasis, cholecystitis, and pancreatitis Flashcards

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
Q

obstruction

A

chemical irritation
mechanical irritation
ischaemia
superimposed infection eg. e coli, enterococcus, klebsiella, and enterobacter

26
Q

what is released in response to gallbladder inflammation

A

inflammatory mediators which further propagate inflammation

27
Q

chemical irritation

A

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
Q

acute acalculous cholecystitis develops in

A

5-10% of patients that udergo cholecystectomy

29
Q

associated conditions in acute acalculous cholecystitis

A

trauma, non-biliary surgery, sepsis, bruins, parenteral nutrition, mechanical ventilation, multiple blood transfusions, prior uses of narcotics or AB

30
Q

mechanisms of acute acalculous CS

A

bile stasis and increased viscosity resulting in obstruction, mucosal ischaemia, infection, external obstruction of biliary tree

31
Q

clinical symptoms of acute acalculous CS

A

smilar to calculous but may be insidious and masked by the precipitating/associated conditions
incidence of gangrene and perforation is higher

32
Q

clinical presentation of of cholecystitis

A 
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
Q

investigations of cholecystitis

A

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
Q

histology of cholecystitis

A 
mucosal damage - ulceration 
inflammation - acute/chronic 
mucosal regeneration with hyperplasia 
fibrosis (repair) 
muscle hypertrophy 
diverticula
35
Q

treatment of cholecystitis

A

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
Q

why should surgery be done 2-3 days after onset of symptoms

A

after this period, development off adhesions and transmural inflammation increases risk of complications

37
Q

chronic cholecystitis

A

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
Q

mechanism of chronic cholecystitis

A

similar to acute cholecystitis

supersaturation of bile leading to chronic inflammation and stone formation

39
Q

macroscopic findings in chronic cholecystitis

A

serosa may be dulled, fibrous adhesions, churned and fibrotic, wall this or thick, attenuated and trabeculated muscosa

40
Q

pancreas

A

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
Q

parts of the pancreas

A

head, uncinate, neck, body and tail

42
Q

two histological components of the pancreas

A

endocrine and exocrine

43
Q

pancreas divism

A

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
Q

acute pancreatitis

A

reversible pancreatic injury associated with inflammation

common

45
Q

aetiological factors of acute pancreatitis

A
  • 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
Q

mechanism of pancreatitis

A

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
Q

consequences of pancreatitis

A

fat necrosis, interstitial inflammation, vascular damage and haemorrhage, parenchymal necrosis

48
Q

fat necrosis

A

release of fatty acids, which bind calcium and magnesium ions to form insoluble soaps (fat saponification)

49
Q

clinical presentation of pancreatitis

A

20% severe
severe cases - shock with multi organ failure due to release of toxic enzymes, cytokines and the inflammatory mediators into circulation

50
Q

diagnosis of acute pancreatitis

A

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
Q

investigations for acute pancreatitis

A
  • 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
Q

local complications of acute pancreatitis

A
  • peripancreatic fluid collection
  • pseudocyst
  • necrotic collection
  • gastric outlet dysfunction
  • splenic and portal vein thrombosis
53
Q

systemic complications of acute pancreatitis

A
  • exacerbation of pre-existing co morbidity

- organ failure

54
Q

chronic pancreatitis

A

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
Q

clinical presentation of chronic pancreatitis

A
  • 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
Q

hereditary pancreatitis

A

characteristically

  • recurrent bouts of pancreatitis beginning in childhood
  • gremlin mutation neither result in enhances activation of trypsin or inhibit/impede its inactivation
57
Q

autoimmune pancreatitis

A

mass forming inflammatory lesion of the pancreas - may mimic cancer
other times, is a diffuse radiological/macroscopic abnormality of pancreas identified

58
Q

two clinicopathological subtypes of autoimmune apocreatitis

A
  • type 1 - IgG4 related disease

- type 2 - not IgG4 related, usually associated with IBD

59
Q

treatment for autoimmune pancreatitis

A

steroids

60
Q

aetiology of autoimmune pancreatitis

A

multifactorial - genetic factors, bacterial infection, autoimmunity

pathology 2 (47 decks)

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