Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Liver, Biliary Tract & Pancreas > Flashcards

Liver, Biliary Tract & Pancreas Flashcards

1
Q

What is the causative agent of Hepatitis A? Describe the clinical course of Hepatitis A infection. How do serological markers change with time in Hepatitis A infection? How does the community prevalence of Hepatitis A differ from developed and developing countries?

A
  1. Hepatitis A
    - Single-stranded RNA picornavirus
  2. Clinical course of Hepatitis A infection
    - Spread by faecal-oral route
    - Incubation period of 2 - 6 weeks
    - Self-limiting disease
    - Symptoms presenting as fever, vomiting, diarrhoea, lethargy
    - No chronic or carrier state
    - Not associated with hepatocellular carcinoma
    - Rarely causes fulminant hepatitis
    - Low mortality rate at 0.1%
  3. Serological markers in Hepatitis A infection
    - Incubation period = Nothing detected
    - After incubation period, faecal HAV levels rises acutely
    - In the acute phase, IgM anti-HAV levels rises when HAV levels peak
    - IgM levels rises over 2 - 12 weeks and then slowly drops over months
    - As IgM levels drop, IgG anti-HAV levels will rise slowly
    - IgG levels can last for years and confer immunity to the disease
  4. Difference in prevalence of Hepatitis A
    - Developed countries -> Lesser incidence -> 50% of population at age 50yo have serological evidence of infection
    - Developing countries -> Higher incidence -> 100% of population at late teens have serological evidence of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the causative agent of Hepatitis B? How can Hepatitis B infection be transmitted? Describe the pattern of disease progression following Hepatitis B infection. What are the serological findings associated with acute Hepatitis B infection? How may Hepatitis B lead to UGIB? What are the other complications of Hepatitis B-induced cirrhosis?

A
  1. Hepatitis B is caused by
    - Partially double-stranded DNA Hepadnavirus
  2. Transmission of Hepatitis B infection
    - Vertical/congenital -> Most common route
    - Parenteral -> Contaminated blood products, blood transfusions, needle stick injury, sharing of needles in IVDU
    - Body fluids -> Sexual
  3. Hepatitis B disease progression
    - Incubation period 1 - 4 months
    - Asymptomatic carrier state
    - Acute hepatitis -> Subclinical disease (70%) or icteric disease (30%)
    + Recover (90%)
    + Fulminant hepatitis (<0.5%)
    + Chronic hepatitis (5%)
    > Non-progressive chronic hepatitis
    > Progressive chronic hepatitis -> Cirrhosis -> Hepatocellular CA
  4. Serological findings in acute Hepatitis
    - HBsAg
    - HBcAg
    - HBeAG
    - IgM anti-HBc
    - IgM anti-HBe
    - HBV DNA PCR
  5. UGIB in Hepatitis B caused by
    - Liver cirrhosis -> Portal HTN -> Oesophageal varices
    - Coagulopathy due to reduced liver synthetic function
  6. Hepatitis B cirrhosis complications
    - Hepatic encephalopathy
    - Jaundice
    - Hepatorenal syndrome
    - Ascites
    - Pleural effusions
    - Splenomegaly
    - Hypogonadism
    - Hepatocellular CA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of virus causes Hepatitis C? What are the risk factors for acquiring Hepatitis C? What is the natural course for Hepatitis C? What serological markers can be picked up with Hepatitis C? What features of the Hepatitis C virus makes vaccine development difficult?

A
  1. Hepatitis C is caused by
    - Single-stranded RNA flavivirus
  2. Risk factors for Hepatitis C
    - Vertical transmission -> Mother with Hepatitis C infection
    - IVDU
    - Multiple sexual partners
    - Healthcare workers
    - Needle stick injury
    - Blood transfusion in the older days
  3. Natural course of Hepatitis C
    - Incubation period of 2 - 26 weeks
    - Acute hepatitis C -> Asymptomatic or mild disease
    + Persistent chronic hepatitis (80%)
    > Cirrhosis (20%) -> Death, hepatocellular carcinoma
    > Non-progressive chronic hepatitis (80%).
    + Recovery/resolution (10 - 15%)
    + Fulminant hepatitis (Rare)
  4. Serological markers in Hepatitis C
    - Incubation period 2 - 26 weeks -> Nothing detectable
    - Acute infection
    + HCV DNA detectable in 1 - 3 weeks
    + Shortly after anti-HCV IgM/IgG detectable during acute infection
    - Chronic
    + IgM levels drop but IgG levels persist
    - Presence of IgG does not confer immunity
  5. Vaccination difficult in Hepatitis C due to
    - Hepatitis C virus with stable core but variable envelope
    - RNA polymerase is unstable with frequent mutations
    - Genomic and antigenic variability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the Hepatitis D virus. How does Hepatitis D causes hepatitis? How is Hepatitis D infection diagnosed?

A
  1. Hepatitis D virus
    - Circular defect single-stranded RNA virus
    - Deltaviridae family
    - Due to defect it requires HBsAg to encapsulate it as its outer coat before it can replicate to cause infection
  2. Hepatitis D always occur concurrently with Hepatitis B infection
    - Acute co-infection with HBV -> HBV + HDV is transmitted together -> HBV replicates first and cause infection -> HBsAg to encapsulate HDV -> HDV virus replicates to cause infection
    - Super-infection in chronic HBV individuals causing
    + Severe acute hepatitis in undiagnosed asymptomatic HBV carrier
    + Converts mild chronic hepatitis B into fulminant hepatitis or progressive cirrhosis
  3. Serology in Hepatitis D infection
    - HDV DNA
    - IgM anti-HDV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the causes of jaundice? Apart from jaundice, what are the clinical features of hepatic failure? Outline the normal metabolism and elimination of bilirubin.

A
  1. Causes of jaundice
    A. Unconjugated hyperbilirubinaemia
    - Pre-hepatic
    + Increased bilirubin production -> Hemolytic anaemia, thalassemia
    - Hepatic
    + Reduce hepatic uptake -> Gilbert’s syndrome
    + Impaired conjugation -> Hepatitis, physiological jaundice of newborn
    B. Conjugated hyperbilirubinaemia
    - Post-hepatic
    + Reduced bile outflow -> Choledocholithiasis, pancreatic head CA, cholangitis
  2. Clinical features of hepatic failure
    - Portal hypertension -> Oesophageal varices, UGIB
    - Coagulopathy
    - Pruritus
    - Hepatorenal syndrome
    - Hepatic encephalopathy
    - Ascities
    - Pleural effusion
    - Hypogonadism
  3. Bilirubin
    - Produced from breakdown of haem from RBC
    - Unconjugated bilirubin is insoluble
    - Bound to albumin to be transported to liver
    - Uptake into liver
    - Undergoes glucuronidation to become conjugated bilirubin
    - Excreted as bile into gut
    - Deconjugated in gut to become urobilinogen
    - 20% of urobilinogen reabsorbed into enterohepatic circulation
    - Some urobilinogen excreted in urine as urobilin (yellow)
    - Some urobilinogen broken down by gut bacteria into stercobilin (brown) to be excreted in faeces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of pancreatitis? What is the likely pathogenesis of acute pancreatitis? What are the acute complications of severe pancreatitis? What are the laboratory findings in acute pancreatitis? Describe the cellular morphology of acute pancreatitis

A
  1. Causes of pancreatitis *I GET SMASHED
    - Idiopathic
    - Gallstones
    - ETOH
    - Trauma
    - Steroids
    - Mumps
    - Autoimmune disease
    - Scorpion stings
    - Hypercalcemia, hypertriglyceraemia
    - ERCP
    - Drugs
  2. Pathogenesis of acute pancreatitis
    - Autodigestion of pancreas due to inappropriate secretion of pancreatic enzymes -> Trypsinogen which is activated to trypsin
    - Occurs via 3 mechanisms:
    + Pancreatic duct obstruction -> Gallstones -> Lipase to accumulate and spill out
    + Primary acinar cell injury -> Drugs, ETOH, trauma, mumps, infection
    + Defective intracellular transport of proenzymes in acinar cells
    - Causes interstitial edema and inflammation, fat necrosis, hemorrhage and proteolysis
  3. Acute complications of severe pancreatitis
    - SIRS and shock
    - ARDS
    - DIC
    - Hemolysis
    - Pseudocyst
    - Hemorrhage
  4. Laboratory findings in acute pancreatitis
    - Raised serum amylase within 24 hours
    - Raised serum lipase within 72 - 96 hours
    - Hypocalcemia -> Poor prognostic sign
    - Raised WCC
    - Raised CRP
    - Glycosuria
  5. Cellular morphology of acute pancreatitis
    - Interstitial edema and inflammation
    - Fat necrosis
    - Hemorrhage
    - Proteolysis of parenchyma
    - Lipolysis by enzymes
    - Fatty acids combine with calcium to form calcium soap
    - Red black hemorrhages mixed with yellow white necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the morphological features of chronic pancreatitis? What are the clinical consequences?

A
  1. Morphology of chronic pancreatitis
    - Parenchyma fibrosis
    - Calcification
    - Variable number and size of acinar cells
    - Sparing of islet of Langerhans
    - Pancreatic duct obstruction
    - Damage to exocrine parenchyma +/- endocrine parenchyma
  2. Clinical consequences of chronic pancreatitis
    - Irreversible impairment of pancreatic function leading to diabetes, steatorrhea, malabsorption
    - Pseudocyst -> Infected
    - No rise in lipase/amylase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of portal HTN? What are the clinical consequences of portal HTN? What mechanisms are involved in the formation of ascites?

A
  1. Causes of portal HTN essentially is due to increased resistance of portal blood flow
    - Prehepatic -> Portal vein thrombosis
    - Hepatic -> Cirrhosis, massive fatty liver
    - Posthepatic -> Severe RHF, constrictive pericarditis
  2. Clinical consequences of portal HTN
    - Ascites
    - Porto-systemic shunts -> Oesophageal varices, haemorrhoids, spider naevi
    - Hepatic encephalopathy
    - Hepatorenal syndrome
    - Congestive splenomegaly
  3. Mechanisms causing ascites in portal HTN
    - Sinusoidal HTN -> Increased hydrostatic pressure and reduced oncotic pressure from hypoalbuminaemia -> Starling’s forces -> Transudate into peritoneum
    - Increased hepatic lymph production -> Exceeds thoracic duct drainage capacity -> Spills into peritoneum
    - Splanchnic vasodilation -> Decreased BP -> Renal retention of water and sodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the pathological features of the liver in alcoholic liver disease. Which of these features are reversible? What are the possible sequelae of cirrhosis?

A
  1. Pathological features of alcoholic liver disease
    - Hepatic steatosis -> Fatty changes in liver
    - Hepatitis -> Inflammation, Mallory bodies, liver cell necrosis
    - Cirrhosis -> Extensive fibrosis
    - Hepatocellular carcinoma
  2. Hepatic steatosis and hepatitis are reversible
    - Cirrhosis is irreversible
  3. Consequences of liver cirrhosis
    - Portal HTN -> Thrombo-systemic shunts -> Esophageal varices -> UGIB
    - Coagulopathy
    - Hypoalbuminaemia
    - Ascites
    - Pleural effusion
    - Hepatic encephalopathy
    - Hepatorenal syndrome
    - Congestive splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the pathogenesis of acute calculous cholecystitis. What are the complications of cholecystitis? How does acalculous cholecystitis differ? What conditions are associated with acute acalculous cholecystitis? Describe the clinical features of acute cholecystitis. How do the clinical features of acute calculous cholecystitis differ from acalculous cholecystitis?

A
  1. Acute calculous cholecystitis is due to gallbladder obstruction leading to chemical irritation
    - Gallstone blocks gallbladder outlet
    - Mucosal phospholipases acts on lecithin converting it to toxic lysolecithin
    - Disrupts protective glycomucosal layer of gallbladder
    - Exposes gallbladder wall epithelium to actions of bile salts
    - Inflammation due to prostaglandin
    - Gallbladder dysmotility
    - Distension, increase intraluminal pressure and reduced blood flow
    - Stasis which encourages bacteria infection -> Cholecystitis
  2. Complications of cholecystitis
    - Bacteria infection -> Cholangitis and sepsis
    - Gallbladder perforation and localised abscess
    - Gallbladder perforation and peritonitis
    - Gallbladder fistula
    - Porcelain Gallbladder
  3. Acalculous cholecystitis
    - Rarer
    - Usually in predisposed individuals
    - Slower/insidious onset
    - Due to ischaemia of cystic end arteries
    - Contributory factors -> sludging micro-crystals, stasis, inflammation, distension
  4. Conditions associated with acalculous cholecystitis
    - Post-major surgery
    - Severe burns
    - Severe trauma
    - Sepsis
    - Vasculitis
    - Postpartum
  5. Clinical features of acute cholecystitis
    - RUQ pain
    - Murphy’s sign +ve
    - Fever
    - N+V
    - Anorexia
    - Chills and rigors
  6. Acute calculous vs acalculous cholecystitis
    - Calculous -> Sudden onset, gallstones
    - Acalculous -> Insidious onset, associated with post-major surgery, sepsis, severe trauma, severe burns, higher risk of complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly

Pathology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions