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ACEM Primary Written > Gastroenterology: Pathology - Liver > Flashcards

Gastroenterology: Pathology - Liver Flashcards

1
Q

Describe the relative proportions of the liver’s dual blood supply

A

60-70% portal venous
30-40% hepatic artery

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2
Q

How and where do the portal vein and hepatic artery enter the liver?

A

At the inferior surface via transverse fissure (porta hepatitis)

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3
Q

Describe the lobular model of the liver

A

Liver divided into 1-2mm hexagonal lobules oriented around the terminal hepatic veins, with portal tracts at the periphery
Hepatocytes are described as either centrilobular or periportal

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4
Q

Describe the acinar model of the liver. What are the three zones of the liver in the acinar model?

A

Apex of acini at hepatic vein with base formed by septal venules of the portal vein
Divided into three zones:
1. Closest to vascular supply (base of acinus)
2. Intermediate
3. Most remote from afferent blood supply (apex, abutting terminal hepatic vein)

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5
Q

How are hepatocytes organised within the liver architecture? Where are the bile ducts found?

A

In cribiform plates with vascular sinusoids in between
Between abutting hepatocytes are bile canaliculi

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6
Q

How does bile drain from the liver?

A

Bile canaliculi between hepatocytes -> canals of Hering -> bile ductules -> terminal bile ducts (in portal tracts)

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7
Q

What % of hepatic functional capacity must be lost before hepatic failure ensues?

A

80-90%

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8
Q

What is the mortality of hepatic failure without transplantation?

A

~80%

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9
Q

What are three types of hepatic failure? Which is most common?

A
  1. Acute liver failure
  2. Chronic liver disease*
  3. Hepatic dysfunction without overt necrosis
  • most common
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10
Q

What is the most common cause of acute liver failure?

A

Paracetamol toxicity

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11
Q

Define acute liver failure. What constitutes fulminant and sub-fulminant failure?

A

Acute liver illness associated with encephalopathy within 6 months of initial diagnosis
Fulminant if encephalopathy occurs within 2 weeks of onset of jaundice
Sub-fulminant if encephalopathy occurs within 3 months of onset of jaundice

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12
Q

What causes acute liver failure?

A

Massive hepatic necrosis (most commonly due to drugs or toxins)

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13
Q

Describe the most common causes of acute liver failure and their relative proportions

A

50% paracetamol toxicity
14%: halothane, antimycobacterial drugs (rifampin, isoniazid), MAOIs, industrial chemical, mushroom poisoning
8% HBV
4% HAV

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14
Q

Give two examples of causes of hepatic dysfunction without overt necrosis

A
  1. Tetracyclines
  2. Acute fatty liver of pregnancy
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15
Q

Seven clinical features of liver failure and the underlying cause (in brief)

A
  1. Jaundice (hyperbilirubinaemia)
  2. Oedema, ascites (hypoalbuminaemia)
  3. Encephalopathy (hyperammoniaemia)
  4. Fetor hepaticus (increased mercaptans, portosystemic shunt)
  5. Palmar erythema, spider naevi, gynaecomastia, hypogonadism (hyperoestrogenaemia)
  6. Coagulopathy (decreased clotting factors) -> other sequelae including GI bleeding (especially variceal due to portal HTN)
  7. Hepatorenal and hepatopulmonary (complex and uncertain mechanism)
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16
Q

Describe the three morphological features of cirrhosis

A
  1. Fibrosis: bridging fibrous septa
  2. Parenchymal nodules: regenerating hepatocytes encircled by fibrosis
  3. Disruption of hepatic architecture: diffuse
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17
Q

What are the three central processes involved in the pathogenesis of cirrhosis?

A
  1. Hepatocyte death
  2. ECM deposition
  3. Vascular reorganisation
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18
Q

Describe the changes in connective tissue deposition in cirrhosis. What cells are responsible for this connective tissue deposition?

A

Normally type I and III collagens are concentrated in portal tracts and around central veins, with strands of type IV in space of Disse
In cirrhosis, type I and III collagens are deposited in space of Disse creating fibrotic septal tracts and obliterating sinusoidal fenestrations (“capillarisation”)
Sinusoids lose capacity for solute exchange with hepatocytes

Due to action of perisinusoidal stellate cells (Ito cells)

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19
Q

What four factors stimulate Ito cells to increase ECM deposition?

A
  1. Chronic inflammation (TNF, lymphotoxin, IL-1B, lipid peroxidation products)
  2. Cytokines and chemokines (released by Kupffer cells, endothelial cells, hepatocytes, bile duct epithelial cells)
  3. ECM disruption
  4. Direct stimulation by toxins
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20
Q

Five broad causes of cirrhosis with examples of each

A
  1. Toxins:
    - Alcohol
    - Drugs (e.g. amiodarone, methyldopa, methotrexate)
  2. Metabolic:
    - Non-alcoholic steatohepatitis
    - Alpha-1-antitrypsin deficiency
    - Haemochromatosis
    - Wilson disease
  3. Infectious:
    - HBV, HCV
  4. Autoimmune:
    - Primary biliary cirrhosis
    - Primary sclerosing cholangitis
  5. Vascular:
    - Budd-Chiari
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21
Q

What are the three most common causes of cirrhosis?

A

Alcohol abuse (most common; 60-70%)
Viral hepatitis (10%)
Non-alcoholic steatohepatitis (10-15%)

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22
Q

Two prehepatic causes of portal HTN

A
  1. Portal vein thrombosis or narrowing
  2. Massive splenomegaly with shunting of blood into splanchnic circulation
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23
Q

Six intrahepatic causes of portal HTN

A
  1. Cirrhosis (most common)
  2. Schistosomiasis
  3. Veno-occlusive disease
  4. Massive fatty change
  5. Diffuse fibrosing granulomatous disease
  6. Nodular regenerative hyperplasia
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24
Q

Three posthepatic causes of portal HTN

A
  1. Severe RHF
  2. Constrictive pericarditis
  3. Hepatic vein outflow obstruction (Budd-Chiari syndrome)
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25
Q

What is ascites and what is the most common cause?

A

Accumulation of excess serous fluid in peritoneal cavity
85% caused by cirrhosis

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26
Q

At what level is ascites clinically detectable?

A

Above 500ml

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27
Q

Describe the typical composition of ascitic fluid

A

Serous with <3g/dL protein and serum:ascites albumin of >1.1g/dL
Similar concentration of solutes to blood
May contain scant mesothelial cells and mononuclear lymphocytes
Neutrophils suggest secondary infection, and blood suggested disseminated cancer

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28
Q

What three factors are involved in the pathogenesis of ascites?

A
  1. Altered Starling’s forces: increased hydrostatic pressure due to sinusoidal HTN, and decreased oncotic pressure due to hypoalbuminaemia
  2. Increased hepatic lymph flow: overwhelms thoracic duct drainage
  3. Increased splanchnic capillary pressure: due to RAAS activation and ADH release stimulated by initial splanchnic vasodilation (results in vasoconstriction, and increased Na+ and fluid retention)
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29
Q

Describe the composition of hepatic lymph

A

Protein-rich
Low in triglycerides

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30
Q

At what three sites do portosystemic shunts develop and how does this manifest clinically?

A
  1. Rectum: haemorrhoids
  2. Oesophagogastric junction: varices
  3. Falciform ligament and umbilicus: caput medusae
  4. Retroperitoneum
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31
Q

What causes the thrombocytopaenia (+/- pancytopaenia) seen with portal HTN?

A

Congestive splenomegaly

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32
Q

What are the four major clinical consequences of portal HTN?

A
  1. Ascites
  2. Portosystemic venous shunts
  3. Congestive splenomegaly
  4. Hepatic encephalopathy
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33
Q

When does jaundice occur?

A

When bilirubin production exceeds hepatic clearance

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34
Q

Outline the five steps of normal bilirubin formation and metabolism

A
  1. Haem from senescent erythrocytes converted to biliverdin by haem oxygenase in mononuclear phagocytes
  2. Biliverdin reductase in mononuclear phagocytes further catalyses the conversion of biliverdin to bilirubin, which is then tightly complexed with albumin for transport to the liver
  3. Carrier-mediated uptake of bilirubin occurs at sinusoidal membrane
  4. Within hepatocytes, bilirubin is conjugated to 1-2 molecules of glucuronic acid by the enzyme UDP glucuronyl transferase (UGT1A1): conjugates are water-soluble and readily excreted in bile
  5. Bacterial B-glucuronidases in the gut deconjugate bilirubin to form urobilinogen
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35
Q

What % of normal bile formation is due to erythrocyte breakdown? Where does this occur? What process is responsible for the remaining % of normal bile formation?

A

85% due to RBC breakdown by mononuclear phagocytic system (especially in liver, spleen and bone marrow)

15% from tumour of hepatic haem or haemoproteins (e.g. CYP450 enzymes), and from premature destruction of RBC precursors in bone marrow

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36
Q

What is the fate of urobilinogen in the gut?

A

Majority excreted in faeces
20% reabsorbed in ileum and colon and returns to liver to be re-excreted in bile
Small amount of reabsorbed urobilinogen is excreted in the urine

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36
Q

Describe the colours of the various bilirubin metabolites

A

Biliverdin: green
Bilirubin: yellow-brown
Urobilinogen: colourless

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37
Q

Mutations in UGT1A1 are responsible for what forms of hyperbilirubinaemia? Give two examples

A

Heredity unconjugated hyperbilirubinaemia
E.g. Crigler-Najjar, Gilbert

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38
Q

What is the major component of bile and how is it formed?

A

Bile salts, formed from bile acids formed from cholesterol

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39
Q

What % of bile salts are reabsorbed following secretion?

A

95% reabsorbed in GIT (“enterohepatic circulation”)

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40
Q

Which bilirubin metabolites are water soluble and which are water insoluble?

A

Unconjugated bilirubin is water-insoluble and tightly complexed with albumin: cannot be excreted in urine
Conjugated bilirubin is water-soluble and loosely albumin-bound: can be excreted in urine

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41
Q

What causes kernicterus?

A

Haemolytic anaemia causes an unconjugated hyperbilirubinaemia
Unbound unconjugated bilirubin fraction increases: this fraction can diffuse into tissues including the brain where it is toxic

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42
Q

What are the two types of hyperbilirubinaemia and what are the broad causes of each?

A

Unconjugated:
1. Excessive extrahepatic production
2. Decreased hepatic uptake
3. Impaired conjugation

Conjugated (cholestatic):
1. Decreased hepatocellular excretion
2. Impaired bile flow

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43
Q

Three examples of causes unconjugated hyperbilirubinaemia due to excessive extrahepatic production

A
  1. Haemolytic anaemias
  2. Resorption of blood from internal haemorrhage (e.g. GIT, haematoma)
  3. Ineffective erythropoiesis (e.g. pernicious anaemia, thalassaemia)
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44
Q

Two examples of causes of unconjugated hyperbilirubinaemia due to decreased hepatic uptake

A
  1. Drug interference with membrane carrier systems (e.g. rifampicin)
  2. Some cases of Gilbert syndrome
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45
Q

Four examples of causes of unconjugated hyperbilirubinaemia due to impaired conjugation

A
  1. Physiological jaundice of newborn (decreased UGT1A1 activity)
  2. Breast milk jaundice (B-glucuronidase in milk)
  3. Genetic deficiency of UGT1A1 (e.g. Crigler-Najjar, Gilbert syndrome)
  4. Diffuse hepatocellular disease (e.g. viral or drug-induced hepatitis, cirrhosis)
46
Q

Give an example of a cause of conjugated hyperbilirubinaemia due to decreased hepatocellular excretion

A

Deficiency of canalicular membrane transporters (e.g. Dubin-Johnson syndrome, Rotor syndrome)

47
Q

What % of bilirubin must be conjugated in hyperbilirubinaemia for it to be considered conjugated hyperbilirubinaemia?

A

> 50%

48
Q

What is cholestasis?

A

A pathologic condition of impaired bile formation and flow
Symptoms include jaundice, pruritis, skin xanthomas (due to focal accumulation of cholesterol), or symptoms related to malabsorption syndrome (especially of fat-soluble vitamins A, D, E, K)

49
Q

What causes conjugated hyperbilirubinaemia?

A

Cholestasis (either due to decreased hepatocellular excretion of bile or impaired bile flow)

50
Q

Describe the typical course of hepatitis A

A

Benign self-limiting disease with incubation period of 3-6 weeks

51
Q

How is hepatitis A spread?

A

Faecal-oral route, with virus shed in faeces for 2-3 weeks before and 1 week after onset of jaundice

52
Q

What % of acute hepatitis worldwide is caused by hepatitis A?

A

25%

53
Q

What kind of virus is hepatitis A?

A

ssRNA

54
Q

How often does hepatitis A cause:
- Chronic disease
- Carrier state
- Fulminant hepatitis?

A

Does not cause chronic disease or carrier state
Rarely causes fulminant hepatitis

55
Q

Describe the pattern of serum markers seen with hepatitis A infection

A

Acute infection is marked by appearance of anti-HAV IgM in the serum
IgM begins to decline in a few months, with appearance of IgG which persists for years and may confer lifelong immunity

56
Q

What % of those who contract hepatitis B develop symptomatic acute hepatitis in the first instance?

A

30% (70% have asymptomatic subclinical disease)

57
Q

What % of those who contract hepatitis B experience recovery after initial acute illness? What % develop fulminant hepatitis and what % go on to develop chronic hepatitis?

A

90% recover
<0.5% develop fulminant hepatitis
<5% progress to chronic hepatitis

58
Q

What % of chronic hepatitis B sufferers recover? What % become healthy carriers? What % develop cirrhosis?

A

<2% recover
30% assume healthy carrier state
12-20% develop cirrhosis

59
Q

What % of cirrhotic patients with hepatitis B will develop HCC?

A

6-15%

60
Q

What patient subgroup most commonly assumes a healthy carrier state after developing chronic hepatitis B infection?

A

Children whose infections were contracted perinatally

61
Q

What kind of virus is hepatitis B? What family is it from?

A

dsDNA
Hepadnavirus

62
Q

What is the incubation period of hepatitis B?

A

Typically 6-8 weeks but may be 4-26 weeks

63
Q

What is the common mode of spread of hepatitis B in high-, intermediate-, and low-prevalence areas?

A

High prevalence: perinatal during childbirth
Intermediate prevalence: horizontal during early childhood (skin/mucosal cuts/breaks in children with close bodily contact)
Low prevalence: sexual intercourse, IVDU

64
Q

Five viral antigens of hepatitis B

A
  1. HBcAg: nucleocapsid core protein
  2. HBeAg: longer polypeptide with precore and core regions
  3. HBsAg: envelope glycoproteins
  4. HBx protein: necessary for viral replication
  5. Polymerase with both DNA polymerase and reverse transcriptase activity
65
Q

Describe the change in antigen markers throughout the natural course of hepatitis B

A
  1. HBsAg: appears before onset of symptoms, peaks during overt disease, and is undetectable after 3-6 months
  2. IgM anti-HBc becomes detectable shortly before onset of symptoms (concurrent with onset of transaminitis) and over a period of months is replaced by IgG anti-HBc
  3. HBeAg, HBV DNA, and DNA polymerase appear soon after HBsAg and indicate active viral replication (persistence of HBeAg indicates continued infectivity and probable progression to chronic hepatitis)
  4. Anti-HBs antibody is usually not detectable until weeks to months after disappearance of HBsAg, and may persist for life, conferring protection
  5. Appearance of anti-HBe antibodies implies acute infection has peaked and is waning
66
Q

What kind of virus is hepatitis C? What family is it from?

A

ssRNA
Flavivirus family

67
Q

What % of those with hepatitis C progress to chronic infection? Of these, how many will develop cirrhosis?

A

85% develop chronic infection
Of those with chronic infection, 20-30% will develop cirrhosis

68
Q

Seven risk factors for hepatitis C infection. Which are most common?

A
  1. IVDU (most common; 54%)
  2. Multiple sex partners (36%)
  3. Surgery within last month
  4. Needlestick injury
  5. Multiple contacts with HCV-infected person
  6. Employment in medical or dental fields
  7. Unknown (32%)
69
Q

What is the most common indication for liver transplant?

A

Chronic hepatitis C infection

70
Q

Which has greater risk of perinatal transmission: hepatitis B or C?

A

Hepatitis B (although perinatal transmission still the major mode of transmission of hepatitis C in children)

71
Q

What % of acute hepatitis C infection is asymptomatic? What % of those who contract hepatitis C experience recovery after initial acute infection? What % develop fulminant hepatitis and what % go on to develop chronic hepatitis?

A

During initial infection 85% are asymptomatic
From this acute infection:
- 15% recover
- 85% progress to chronic disease
- Rarely causes fulminant hepatitis

72
Q

Why has it been difficult to develop a hepatitis C vaccine? What does this mean for acquired immunity to hepatitis C?

A

Due to inherent genomic instability and antigenic variability of the virus

Also means that elevated anti-HCV IgG following acute infection does not consistently confer immunity: virus can be reactivated or re-emerge as newly mutated strain to cause repeated bouts of hepatic damage

73
Q

What is the incubation period of hepatitis C?

A

Typically 6-12 weeks (range 2-26 weeks)

74
Q

Describe the change in antigen markers throughout the natural course of hepatitis C

A
  1. HCV RNA detectable for 1-3 weeks during acute infection, coinciding with transaminitis
  2. In symptomatic acute infection, anti-HCV antibodies are only detected in 50-70% of cases; in remainder of patients, antibodies emerge after 3-6 weeks
  3. In chronic infection, circulating HCV RNA persists in >90% of cases and is associated with characteristic episodic transaminitis (with intervening periods of normal or near-normal transaminases)
75
Q

What type of virus is hepatitis D?

A

ssRNA

76
Q

What are the three patterns of infection seen with hepatitis D?

A
  1. Acute co-infection of HBV and HDV
  2. Superinfection: when chronic HBV carrier is newly exposed to HDV
  3. Helper-independent latent infection: in liver transplant setting
77
Q

What is the clinical presentation seen with acute co-infection of HBV and HDV?

A

Acute hepatitis clinically indistinguishable from acute HBV, with similar rates of progression to chronic infection
Elimination of HBV leads to elimination of HDV

78
Q

What is the clinical presentation seen with superinfection of chronic HBV with HDV?

A

Severe acute hepatitis in previously unrecognised HBV carrier, or exacerbation of chronic hepatitis in known HBV carrier
Chronic HDV infection occurs in 80-90% of cases

79
Q

What are the two phases of infection seen in HDV superinfection of chronic HBV carriers?

A

Acute: active HDV replication with suppression of HBV, high ALT
Chronic: decreased HDV replication, increased HBV replication, fluctuating ALT -> progression to cirrhosis, HCC

80
Q

What is helper-independent latent HDV infection?

A

Occurs with liver transplant
HDV is detected in nuclei or graft liver but administration of anti-HBV Ig prevents concomitant HBV infection
Liver disease only ensues if HBV escapes neutralisation

81
Q

Describe the pattern of serological markers seen with HDV infection. How does this differ between acute co-infection and superinfection?

A
  1. HDV RNA detectable just before and in early days of symptomatic illness
  2. IgM anti-HDV appears late and is short-lived
  3. Acute co-infection is marked by IgM to HDV Ag and HBcAg
  4. Superinfection is marked by HBsAg and anti-HDV (both IgM and IgG) which persists for weeks to months
82
Q

How is HDV treated?

A

IFN-alpha

83
Q

How is HDV prevented?

A

With HBV vaccination

84
Q

What kind of virus is hepatitis E? What family is it from?

A

ssRNA
Calcivirus

85
Q

How is hepatitis E transmitted?

A

Faecal-oral route
Water-borne with zoonotic reservoirs

86
Q

Which viral hepatitis causes a 20% mortality rate in pregnant women?

A

Hepatitis E

87
Q

Describe the typical clinical course of hepatitis E

A

Incubation time 6 weeks
Usually benign and self-limiting without progression to chronic liver disease or persistent viraemia
Exception to this is in pregnant women, in which there is a 20% mortality rate

88
Q

Describe the pattern of serological markers seen with hepatitis E infection

A
  1. HEV RNA and virions detectable in stool and blood prior to onset of illness
  2. Transaminitis, clinical illness, and anti-HEV IgM all coincide
  3. Symptoms resolve within 2-4 weeks, and anti-HEV IgM is replaced by IgG
89
Q

Intranasal cocaine increases risk of contracting which form of hepatitis?

A

Hepatitis C

90
Q

What are the three forms of alcohol liver disease?

A
  1. Hepatic steatosis
  2. Alcoholic steatohepatitis
  3. Cirrhosis
91
Q

Describe the microscopic and macroscopic changes seen in hepatic steatosis

A

Microscopic: lipid droplets accumulate in hepatocytes initially as microvesicular globules, with chronic intake form large macrovesicular globules that displace the nucleus to the periphery
Macroscopic: enlarged, soft, yellow liver

92
Q

Four features of alcoholic steatohepatitis

A
  1. Hepatocyte swelling and necrosis: balloon degeneration, particularly centrilobular
  2. Mallory bodies: eosinophilic cytoplasmic clumps of intermediate filament, not specific to alcoholic liver disease
  3. Neutrophilic reaction (accompanied by lymphocytes and macrophages)
  4. Fibrosis (typically sinusoidal and perivenular, occasionally periportal)
93
Q

List six diseases in which Mallory bodies may be present

A
  1. Alcoholic steatohepatitis
  2. NAFLD
  3. Primary biliary cirrhosis
  4. Wilson disease
  5. Chronic cholestasis
  6. HCC
94
Q

What % of alcoholics develop cirrhosis?

A

10-15%

95
Q

What is the aetiology of secondary biliary cirrhosis?

A

Due to extrahepatic bile obstruction (e.g. biliary atresia, gallstones, stricture, pancreatic cancer)

96
Q

What is the sex predilection in secondary vs primary biliary cirrhosis, and primary sclerosing cholangitis?

A

Secondary biliary cirrhosis: none
Primary biliary cirrhosis: female&raquo_space;> male
Primary sclerosing cholangitis: male > female

97
Q

Describe the presentation of intrahepatic bile duct disorders

A

Pruritis
Jaundice
Malaise
Dark urine
Pale stools
Hepatosplenomegaly

98
Q

Describe the laboratory findings seen in secondary biliary cirrhosis

A

Conjugated hyperbilirubinaemia
Increased ALP, bile acids, cholesterol

99
Q

Describe the laboratory findings seen in primary biliary cirrhosis

A

Conjugated hyperbilirubinaemia
Increased ALP, bile acids, cholesterol
Increased IgM auto-antibodies

100
Q

Describe the laboratory findings seen in primary sclerosing cholangitis

A

Conjugated hyperbilirubinaemia
Increased ALP, bile acids, cholesterol
Increased IgM, hypergammaglobulinaemia

101
Q

Describe the three pathologic findings seen in secondary biliary cirrhosis

A
  1. Prominent bile stasis
  2. Bile duct proliferation with surrounding neutrophils
  3. Portal tract oedema
102
Q

Describe the pathologic findings seen in primary biliary cirrhosis

A

Dense lymphocytic infiltrate in portal tracts with granulomatous destruction of bile ducts

103
Q

Describe the two pathologic findings seen in primary sclerosing cholangitis

A
  1. Periductal portal tract fibrosis
  2. Segmental stenosis of extrahepatic and intrahepatic bile ducts
104
Q

What are the two types of gallstones? Which is more common?

A
  1. Cholesterol (more common, 90%)
  2. Pigmented (predominantly bilirubin calcium salts)
105
Q

Eight risk factors for cholesterol gallstones

A
  1. Increased age
  2. Female sex
  3. Oestrogens (OCP, pregnancy)
  4. Clofibrate
  5. Obesity
  6. Rapid weight loss
  7. Gallbladder stasis
  8. Hyperlipidaemia
106
Q

Five risk factors for pigmented gallstones

A
  1. Asian ethnicity
  2. Rural populations
  3. Chronic haemolytic syndromes
  4. Biliary infection (especially with E. coli, Ascaris lumbricoides, liver fluke)
  5. GI disorders (e.g. ileal disease including Crohn’s, ileal resection or bypass, CF with pancreatic insufficiency)
107
Q

Describe the pathogenesis of cholesterol gallstones

A
  1. Bile is supersaturated with cholesterol
  2. Gallbladder hypomotility promote cholesterol nucleation
  3. Nucleation in bile is accelerated
  4. Mucus hypersecretion in gallbladder traps nucleated crystals, which then aggregate into stones
108
Q

Describe the pathogenesis of pigmented gallstones

A
  1. Increased unconjugated bilirubin fraction in the biliary tree (due to conditions like haemolysis that increase unconjugated fraction, or biliary tree infection with organisms that produce B-glucuronidases)
  2. Precipitation of calcium bilirubin salts
109
Q

Eight complications of gallstones. Which is most common?

A
  1. Cholecystitis (most common)
  2. Cholangitis
  3. Empyema
  4. Perforation
  5. Fistulas
  6. Obstructive cholestasis
  7. Pancreatitis
  8. Gallstone ileus
110
Q

What are the three main types of cholecystitis?

A
  1. Acute calculous cholecystitis
  2. Acute acalculous cholecystitis
  3. Chronic cholecystitis
111
Q

Describe the pathogenesis of calculous cholecystitis

A
  1. Initial irritation and inflammation due to bile stasis
  2. Increased mucosal phospholipase activity -> conversion of lecithin to lysolecithin -> toxic to mucosa
  3. Glycoprotein mucous layer breaks down, with exposure of mucosal epithelium to detergent action of bile salts
  4. Prostaglandin release increases mucosal/mural inflammation
  5. Gallbladder dysmotility -> distension, increased pressure -> decreased mucosal blood flow
  6. Later bacterial contamination can develop due to ongoing inflammation and stasis
112
Q

Describe the pathogenesis of acalculous cholecystitis

A

Thought to result from ischaemia, with other pathogenic factors including:
- Dehydration
- Gallbladder sludge/stasis
- Vascular compromise
- Bacterial contamination

113
Q

Five major risk factors for acalculous cholecystitis

A
  1. Sepsis with hypotension and multi-organ failure
  2. Immunosuppression
  3. Major trauma/burns
  4. Diabetes mellitus
  5. Infections (e.g. Salmonella typhi, staphylococci)

ACEM Primary Written (160 decks)

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