11-17 Flashcards
(291 cards)
1
Q
Describe the primary functions of the liver.
A
The liver’s most important jobs include synthesis, detoxication, and excretion.
2
Q
Explain why infarcts in the liver are rare.
A
Infarcts in the liver are rare due to its double blood supply, which allows retrograde arterial flow through accessory vessels and portal venous supply to sustain liver parenchyma.
3
Q
Define hepatic artery thrombosis in the context of liver transplants.
A
Hepatic artery thrombosis is a complication in transplanted livers that can lead to the death of the transplanted liver parenchyma.
4
Q
How can thrombosis of intrahepatic branches affect the liver?
A
Thrombosis or compression of intrahepatic branches of the hepatic artery may result in localized parenchymal infarct.
5
Q
List potential causes of extrahepatic portal vein obstruction.
A
Potential causes include pancreatitis leading to splenic vein thrombosis, thrombogenic diseases, postsurgical thromboses, and cirrhosis.
6
Q
What symptoms can arise from occlusion of the portal vein or its branches?
A
Symptoms include abdominal pain and manifestations of portal hypertension such as esophageal varices.
7
Q
Describe the condition known as ‘nutmeg liver.’
A
Nutmeg liver is a morphology resulting from chronic congestion of the liver, often associated with right-sided cardiac failure.
8
Q
Explain the significance of ‘infarct of Zahn’ in intrahepatic portal vein occlusions.
A
Intrahepatic portal vein occlusions result in a sharply demarcated area of red-blue discoloration called infarct of Zahn, characterized by congestion of sinusoids and atrophy of hepatocytes without necrosis.
9
Q
What is the relationship between cirrhosis and impaired blood flow through the liver?
A
Cirrhosis is the most common cause of impaired blood flow through the liver, as it slows down blood flow and increases the risk for thrombus formation.
10
Q
How does chronic congestion of the liver relate to cardiac failure?
A
Chronic congestion of the liver can occur due to right-sided cardiac failure, such as in cor pulmonale, leading to conditions like nutmeg liver.
11
Q
What happens to a patient with nutmeg liver who develops acute left ventricular failure?
A
If a patient with nutmeg liver develops acute left ventricular failure, they may experience central hemorrhagic necrosis.
12
Q
Identify the hepatic manifestations of systemic circulatory disorders.
A
Hepatic manifestations include passive congestion of the liver (nutmeg liver) and central hemorrhagic necrosis.
13
Q
Describe the manifestations of impaired blood flow through the liver.
A
Manifestations include ascites, esophageal varices, hepatomegaly, and elevated levels of serum transaminases.
14
Q
Explain Budd-Chiari syndrome and its effects on the liver.
A
Budd-Chiari syndrome is a rare condition caused by occlusion of two or more major hepatic veins, leading to liver congestion, hepatomegaly, ascites, and portal hypertension.
15
Q
Identify the risk factors associated with thrombosis in Budd-Chiari syndrome.
A
Risk factors include hypercoagulable states, polycythemia vera, pregnancy, oral contraceptives, hypercoagulability due to cancer, and invasion of cancers like renal cell carcinoma into the hepatic vein.
16
Q
How does the liver appear in cases of Budd-Chiari syndrome?
A
The liver swells, the capsule becomes tense, and it appears red-purplish.
17
Q
Define the histological appearance of the liver in Budd-Chiari syndrome.
A
Histologically, there is centrilobular congestion, known as nutmeg liver appearance, with centrilobular necrosis.
18
Q
What are the clinical findings in patients with Budd-Chiari syndrome?
A
Clinical findings include hepatomegaly, ascites, and abdominal pain.
19
Q
Describe sinusoidal obstruction syndrome and its common causes.
A
Sinusoidal obstruction syndrome, or hepatic veno-occlusive disease, is caused by damage to the sinusoidal epithelium, most commonly due to chemotherapy or radiation.
20
Q
Explain the pathophysiology of sinusoidal obstruction syndrome.
A
Damaged endothelial cells slough off and form thrombi that block sinusoidal flow, leading to RBCs spilling into the space of Disse and causing stellate cell proliferation and fibrosis.
21
Q
What are the clinical presentations of sinusoidal obstruction syndrome?
A
Clinical presentations are similar to Budd-Chiari syndrome, including hepatomegaly, ascites, and portal hypertension.
22
Q
Define neonatal hepatitis and its characteristics.
A
Neonatal hepatitis is a group of disorders in neonates characterized by hepatocellular dysfunction, cholestasis, and conjugated hyperbilirubinemia.
23
Q
Describe the morphological features of neonatal hepatitis.
A
Morphological features include balloonization or focal necrosis of hepatocytes, multinucleated hepatocytes, lymphocytic infiltration in the portal area, and proliferation of bile ducts.
24
Q
List potential causes of neonatal hepatitis.
A
Causes include TORCH infections and metabolic disorders such as alpha-1 antitrypsin deficiency.
25
Describe Alagille syndrome.
Alagille syndrome is an autosomal dominant condition characterized by a reduced number of bile ducts.
26
Explain the causes of cholangitis.
Cholangitis is primarily caused by bacterial infections, often due to obstruction of bile flow, commonly from choledocholithiasis (gallstones in the common bile duct), but can also result from surgery, tumors, or acute pancreatitis.
27
How does ascending cholangitis occur?
Ascending cholangitis occurs when bacteria enter the biliary tract via the Sphincter of Oddi and ascend through the biliary tree, potentially reaching the intrahepatic biliary ducts.
28
List common pathogens associated with cholangitis.
Common pathogens include E. coli and Klebsiella.
29
Define suppurative cholangitis.
Suppurative cholangitis is a severe form of cholangitis where purulent bile expands the bile ducts, increasing the risk of liver abscess formation and sepsis.
30
What are the symptoms of cholangitis?
Symptoms of cholangitis include fever, chills, abdominal pain, and jaundice.
31
Describe the treatment options for cholangitis.
Treatment for cholangitis includes the administration of antibiotics and drainage of the bile ducts.
32
Explain the difference between direct and indirect hepatotoxic substances.
Direct hepatotoxic substances cause liver damage through their metabolites in a dose-dependent manner, while indirect hepatotoxic substances can initiate immune reactions or alter liver metabolism without a predictable dose-response relationship.
33
List examples of direct hepatotoxic substances.
Examples of direct hepatotoxic substances include anabolic steroids, amantin, contraceptives, tetracyclines, methotrexate, paracetamol (acetaminophen), and alfa-methyl-DOPA.
34
What factors influence the risk of drug-induced liver injury?
Factors influencing the risk of drug-induced liver injury include the dose of the drug, individual susceptibility, and the presence of pre-existing liver conditions.
35
Describe the onset of symptoms related to direct hepatotoxic substances.
The onset of symptoms from direct hepatotoxic substances is typically short.
36
What role do drugs play in liver injury?
Drugs can be a significant cause of liver injury, with some leading to severe hepatopathies and being withdrawn from the market.
37
How can indirect hepatotoxic substances cause liver damage?
Indirect hepatotoxic substances can cause liver damage by acting as haptens that initiate immune reactions or by altering liver metabolism.
38
Describe the main cause of acute viral hepatitis.
Acute viral hepatitis is primarily caused by hepatitis viruses A to E, as well as Epstein-Barr virus (EBV) and cytomegalovirus (CMV).
39
Explain the symptoms associated with acute hepatitis.
Symptoms of acute hepatitis include hepatic jaundice, dark urine, fever, malaise, and nausea.
40
Define the duration of acute hepatitis.
By definition, acute hepatitis lasts for less than 6 months.
41
How can acute hepatitis progress to chronic hepatitis?
If the infection from hepatitis B or C lasts longer than 6 months, it can progress into chronic hepatitis.
42
What are the clinical syndromes that can result from hepatitis virus infections?
Clinical syndromes include asymptomatic acute infection, acute hepatitis, fulminant hepatitis, chronic hepatitis, and chronic carrier state.
43
Describe the gross changes observed in the liver during acute viral hepatitis.
The gross changes include an enlarged and reddened liver.
44
What microscopic changes occur in the liver parenchyma during acute viral hepatitis?
Microscopic changes include ballooning degeneration of hepatocytes, necrosis of hepatocytes, loss of normal architecture, regenerative changes, accumulation of cellular debris in Kupffer cells, and infiltration of mononuclear cells.
45
How does acute hepatitis differ from chronic hepatitis in terms of necrosis and inflammation?
Acute hepatitis causes more necrosis and less inflammation compared to chronic hepatitis.
46
Identify the transmission methods for different types of hepatitis viruses.
Hepatitis A (HAV) and E (HEV) are transmitted via fecal-oral route, while Hepatitis B (HBV), C (HCV), and D (HDV) are transmitted through blood and body fluids.
47
What is the typical resolution process for acute viral hepatitis?
Acute viral hepatitis usually resolves by itself, but infections from Hepatitis B and C can become chronic.
48
Explain the significance of serology in distinguishing the source of acute hepatitis.
The source of acute hepatitis can only be distinguished by serology, which identifies the specific hepatitis virus involved.
49
What is the relationship between liver enzymes ALT and AST in acute hepatitis?
In acute hepatitis, liver enzymes ALT and AST are elevated, with ALT typically being higher than AST.
50
Describe the condition known as fulminant hepatitis.
Fulminant hepatitis is characterized by massive hepatic necrosis and liver failure.
51
What happens to the liver architecture during acute viral hepatitis?
There is a loss of normal architecture in the liver during acute viral hepatitis.
52
How do regenerative changes manifest in the liver during acute hepatitis?
Regenerative changes manifest as hepatocyte proliferation in response to liver injury.
53
Describe the typical progression of hepatitis caused by hepatitis A or E.
Hepatitis caused by hepatitis A or E is usually benign and self-limiting, with an incubation period of 2 to 6 weeks. It does not progress into chronic hepatitis or a carrier state.
54
Explain how hepatitis A and E are transmitted.
Hepatitis A and E are transmitted via the faecal-oral route, primarily through the ingestion of contaminated water or food, such as shellfish from contaminated sources.
55
Identify the primary symptoms experienced during the pre-icteric phase of hepatitis A and E.
During the pre-icteric phase of hepatitis A and E, symptoms include fever, nausea, and vomiting.
56
What is the diagnostic marker for hepatitis A virus (HAV) infection?
The diagnostic marker for HAV infection is the presence of anti-HAV IgM antibodies.
57
Define the term 'fulminant hepatitis' in the context of hepatitis E.
Fulminant hepatitis refers to a severe form of hepatitis E infection that can occur in pregnant women, leading to extensive liver necrosis and potentially requiring a liver transplant.
58
How does the hepatitis B virus (HBV) spread?
HBV spreads through sexual contact, blood, body fluids, and vertically from mother to fetus.
59
Describe the resilience of the hepatitis B virus.
The hepatitis B virus is tough and can withstand extreme temperatures and humidity.
60
What percentage of acute hepatitis B cases progress to chronic hepatitis?
Approximately 5-10% of acute hepatitis B cases progress to chronic hepatitis, with higher rates in individuals infected as children.
61
List the three antigens associated with the hepatitis B virus.
The three antigens associated with the hepatitis B virus are HBsAg, HBeAg, and HBcAg.
62
Explain the difference between IgM and IgG antibodies in the context of hepatitis infection.
IgM is the first antibody that appears in response to infection, while IgG appears later, indicating a more established immune response.
63
Describe the role of T-cell mediated damage in hepatitis A infection.
In hepatitis A infection, liver injury is more likely a result of T-cell mediated damage to infected hepatocytes rather than direct toxicity from the virus.
64
What is the significance of HEV Ag in hepatitis E diagnosis?
HEV Ag can be detected during active infection of hepatitis E, serving as a diagnostic marker.
65
Explain the potential consequences of hepatitis E infection for pregnant women.
Pregnant women infected with hepatitis E can develop fulminant hepatitis, leading to severe liver damage and potentially necessitating a liver transplant.
66
What are the common symptoms that appear after the pre-icteric phase in hepatitis A and E?
After the pre-icteric phase, symptoms such as jaundice, dark urine, and pale stool appear during the icteric phase.
67
Describe the acute disease phase of hepatitis.
During the acute disease phase, icterus develops, and the condition is classified as acute hepatitis. In this phase, HBsAg, HBeAg, and IgM anti-HBc are present in the serum, indicating an active infection.
68
Explain the role of anti-HBc antibodies during acute hepatitis.
Anti-HBc antibodies are produced to fight the virus during the acute hepatitis stage, helping the immune system respond to the infection.
69
Define the convalescence phase in hepatitis.
The convalescence phase is characterized by the disappearance of all antigens from the blood, while IgG anti-HBs and anti-HBc remain, indicating that the person has developed immunity against the virus.
70
How can the presence of anti-HBs indicate immunity in hepatitis patients?
The presence of anti-HBs indicates that the person has successfully fought off the virus and is now immunized against future infections.
71
What happens if hepatitis progresses into chronic infection instead of convalescence?
If hepatitis progresses into chronic infection, HBsAg and HBeAg will remain in the blood, and there will be no anti-HBs present.
72
Describe the transmission route for hepatitis C.
The major route for transmission of hepatitis C is through blood, with intravenous drug use involving previously used needles being the most common method of transmission.
73
Explain the characteristics of the hepatitis C virus (HCV).
HCV is a positive-sense single-stranded RNA virus belonging to the Flaviviridae family, known for its high genetic variability, which complicates vaccine development.
74
What is the typical incubation period for acute hepatitis C?
The incubation period for acute hepatitis C typically ranges from 6 to 12 weeks.
75
How can acute hepatitis C be asymptomatic?
The onset of acute hepatitis C can be asymptomatic, making it easily missed by patients and healthcare providers.
76
What immune responses are involved in clearing HCV infection?
Strong immune responses involving CD4+ and CD8+ cells can lead to a self-limiting infection, but only a minority of patients are able to clear the HCV infection after acute hepatitis.
77
Define the unique characteristic of the HDV virus.
HDV is unique because it cannot cause infection without being encapsulated by HBsAg, meaning it requires HBV coinfection to replicate.
78
Explain the two settings in which HDV infection can occur.
HDV infection can occur in two settings: 1) Coinfection, where a person is exposed to both HBV and HDV simultaneously, and 2) Superinfection, where a person already infected with HBV becomes infected with HDV, which can accelerate the progression to chronic hepatitis.
79
Define chronic hepatitis.
Chronic hepatitis is defined by the presence of symptomatic, biochemical, or serological evidence of continuing or relapsing hepatic disease for more than 3-6 months.
80
Explain the significance of histological findings in chronic hepatitis.
Histological findings are important to document chronic hepatitis, typically requiring a liver biopsy to assess the condition.
81
Describe the types of hepatitis that can become chronic.
Hepatitis B, C, and D can become chronic, with hepatitis C having a chronicity rate of about 80%, while hepatitis B and D have a chronicity rate of less than 10%.
82
How does acute viral hepatitis progress to chronic hepatitis?
Acute viral hepatitis progresses into chronic hepatitis if the body fails to clear the virus.
83
Identify the risk factors for developing chronic viral hepatitis.
Immunocompromised patients are at a higher risk of developing chronic viral hepatitis.
84
What serological markers indicate chronic hepatitis B infection?
Elevated levels of HBsAg, HBeAg, and IgG anti-HBc indicate chronic hepatitis B infection.
85
How can chronic hepatitis C infection be detected?
Chronic hepatitis C infection can be detected by the presence of anti-HCV antibodies and HCV RNA using ELISA or PCR.
86
Explain the role of biopsy in chronic viral hepatitis.
Biopsy in chronic viral hepatitis can be used for grading and staging the disease.
87
Describe the histological differences between acute and chronic viral hepatitis.
Acute viral hepatitis shows inflammation of the lobules, while chronic viral hepatitis shows inflammation around the portal triads.
88
What are the characteristic features of chronic hepatitis due to hepatitis B infection?
Characteristic features include ground glass hepatocytes and a type of necrosis called piecemeal necrosis.
89
List other causes of chronic hepatitis aside from viral infections.
Chronic hepatitis can also be caused by hepatotoxic drugs, metabolic disorders, α1-antitrypsin deficiency, Wilson disease, autoimmune chronic hepatitis, alcohol, and NAFLD.
90
What symptoms are commonly associated with chronic hepatitis?
Symptoms can include fatigue, anorexia, mild jaundice, hepatomegaly, and spider angiomas.
91
Discuss the potential progression of chronic viral hepatitis.
Any chronic viral hepatitis can develop into cirrhosis, and chronic HBV and HCV infections increase the risk for hepatocellular carcinoma even without cirrhosis.
92
What is the clinical significance of elevated liver enzymes in chronic hepatitis?
Elevated liver enzymes may indicate liver damage, but the symptoms of chronic hepatitis are highly variable and do not predict the outcome.
93
Describe the clinical course of chronic viral hepatitis.
The clinical course of chronic viral hepatitis is highly variable; patients may experience spontaneous remission or may have the disease for life. Some develop cirrhosis rapidly, while others may never develop it.
94
List the major causes of death in chronic viral hepatitis.
The major causes of death in chronic viral hepatitis include cirrhosis, liver failure, hepatic encephalopathy, bleeding from oesophageal varices, and hepatocellular carcinoma.
95
Explain the variability in the progression of chronic viral hepatitis.
The progression of chronic viral hepatitis varies significantly among patients, with some experiencing spontaneous remission and others facing lifelong disease, rapid cirrhosis development, or no cirrhosis at all.
96
Do patients with chronic viral hepatitis always develop cirrhosis?
No, not all patients with chronic viral hepatitis develop cirrhosis; some may never develop it.
97
How can chronic viral hepatitis lead to death?
Chronic viral hepatitis can lead to death through several complications, including cirrhosis, liver failure, hepatic encephalopathy, bleeding from oesophageal varices, and hepatocellular carcinoma.
98
Describe cirrhosis and its significance in liver disease.
Cirrhosis is a chronic liver disease characterized by the replacement of normal liver tissue with scar tissue, leading to significant morbidity and mortality. It represents an irreversible end-stage of hepatitis and can result in hepatic decompensation and life-threatening complications.
99
Explain the initial symptoms of cirrhosis and how the liver compensates.
Initially, cirrhosis may be asymptomatic as the remaining functional liver tissue compensates for the loss. However, acute insults can lead to decreased liver function and symptoms of hepatic decompensation.
100
Identify the common causes of cirrhosis.
The most common causes of cirrhosis include alcoholic liver disease, chronic viral hepatitis (C, B, or D), metabolic associated fatty liver disease, and conditions like haemochromatosis and autoimmune hepatitis.
101
Define micronodular cirrhosis and its primary cause.
Micronodular cirrhosis, also known as Laennec cirrhosis, is primarily caused by alcoholism and is characterized by small nodules on the liver.
102
Differentiate between micronodular and macronodular cirrhosis.
Micronodular cirrhosis is caused by alcoholism and features small nodules, while macronodular cirrhosis is associated with chronic hepatitis B or C and autoimmune hepatitis, presenting larger nodules.
103
Explain the histological features of cirrhosis.
Histologically, cirrhosis shows pseudolobules separated by fibrosis, which can be distinguished from normal hepatic lobules by the absence of a central vein.
104
Describe the appearance of a liver affected by cirrhosis.
A liver affected by cirrhosis appears brown, shrunken, and nonfatty, composed of cirrhotic nodules.
105
List the significant symptoms of hepatic failure due to cirrhosis.
Significant symptoms of hepatic failure due to cirrhosis include jaundice, ascites, and hepatosplenomegaly.
106
What laboratory findings are indicative of cirrhosis?
Laboratory findings in cirrhosis typically show elevated serum aminotransferases (ALT and AST) and alkaline phosphatase.
107
Explain the role of cirrhosis as a risk factor for hepatocellular carcinoma.
Cirrhosis is an important risk factor for hepatocellular carcinoma due to the continuous necrosis and regeneration of liver tissue, which can lead to malignant transformations.
108
Describe the process of fibrosis in cirrhosis.
In cirrhosis, continuous necrosis and regeneration of liver parenchyma replace functional liver tissue with fibrosis, forming fibrous septa that contribute to the nodular appearance of the liver.
109
Identify the types of cirrhosis based on their causes.
Types of cirrhosis include micronodular cirrhosis (alcoholism), macronodular cirrhosis (chronic hepatitis B or C, autoimmune hepatitis), pigment cirrhosis (haemochromatosis, Wilson disease), and biliary cirrhosis (damage to the biliary tree).
110
Describe hyperbilirubinemia and its significance in liver failure.
Hyperbilirubinemia is an elevated level of bilirubin in the blood, often leading to jaundice. It indicates impaired liver function, as the liver is unable to process and excrete bilirubin effectively.
111
Explain the relationship between hypoproteinaemia and liver function.
Hypoproteinaemia refers to low levels of proteins in the blood, particularly albumins and globulins. It occurs in liver failure due to the liver's decreased ability to produce these proteins, leading to complications like edema and ascites.
112
Define hepatic failure and its types.
Hepatic failure, or hepatic decompensation, is a condition where the liver cannot perform its normal functions due to damage or scarring. It can be acute or chronic, with chronic hepatic failure often associated with cirrhosis.
113
How does acute hepatic failure differ from chronic hepatic failure?
Acute hepatic failure occurs suddenly and can be caused by factors like viral hepatitis or drug overdose, while chronic hepatic failure develops gradually, often due to long-term conditions like cirrhosis.
114
Explain the complications associated with hepatic failure.
Complications of hepatic failure include parenchymal decompensation (e.g., hypoproteinaemia, coagulopathy, jaundice, hepatic encephalopathy) and vascular decompensation (e.g., ascites, portal hypertension, oesophageal varices).
115
Describe the effects of alcoholic liver disease on liver health.
Alcoholic liver disease (ALD) encompasses liver conditions resulting from chronic alcohol abuse, leading to liver steatosis, alcoholic hepatitis, and potentially cirrhosis if alcohol consumption continues.
116
What is the significance of hepatitis C in chronic alcoholics?
Hepatitis C is commonly found in chronic alcoholics and can accelerate the progression of alcoholic liver disease, increasing the risk of severe liver damage.
117
How does portal hypertension relate to hepatic failure?
Portal hypertension is increased blood pressure in the portal venous system, often resulting from liver scarring in hepatic failure, leading to complications like ascites and oesophageal varices.
118
Explain the term 'hepatorenal syndrome' in the context of liver failure.
Hepatorenal syndrome is a serious complication of liver failure characterized by kidney dysfunction due to impaired blood flow and circulation, often resulting from severe liver disease.
119
Describe the condition known as 'caput medusae' and its association with liver disease.
Caput medusae refers to the appearance of distended and engorged superficial epigastric veins, resembling a medusa's head, often seen in patients with portal hypertension due to liver cirrhosis.
120
Describe the impact of excessive ethanol consumption on chronic liver diseases in Western countries.
Excessive ethanol consumption causes more than 60% of chronic liver diseases in Western countries and is the 5th leading cause of death.
121
Explain the relationship between alcohol consumption and alcoholic liver disease (ALD).
Alcoholic liver disease is caused by significant alcohol consumption over long periods of time, with risk increasing proportionally to the amount consumed.
122
Define the alcohol consumption threshold for developing alcoholic liver disease.
There is no specific threshold for alcohol consumption above which ALD invariably develops, as it varies from person to person, but most individuals with ALD have consumed around 10 units daily for decades.
123
How is a unit of alcohol defined in Europe and the US?
In Europe, one unit of alcohol is defined as 10 g, while in the US it is 14 g.
124
What are some examples of one unit of alcohol?
One unit of alcohol corresponds to one 0.33 L beer, one glass of wine, or one small glass of hard liquor.
125
Discuss the susceptibility of women to alcohol-induced liver injury.
Women are more susceptible to alcohol-induced liver injury compared to men.
126
Explain the potential harms of binge drinking.
Binge drinking may be as harmful as daily drinking in terms of liver health.
127
Describe the process of hepatocellular steatosis.
Hepatocellular steatosis results from shunting substrates away from catabolism towards lipid synthesis due to the high levels of NADH generated from ethanol metabolism.
128
What are the toxic products and metabolites associated with alcoholic hepatitis?
The causes of alcoholic hepatitis include acetaldehyde, reactive oxygen species from ethanol oxidation, cytokine-mediated inflammation, and alcohol itself.
129
Outline the progression of alcoholic liver disease.
The progression of alcoholic liver disease includes hepatocellular steatosis, steatohepatitis, and potentially further liver damage.
130
Define steatosis in the context of liver disease.
Steatosis refers to the fatty change of the liver, where fat accumulates in hepatocytes, particularly in the centrilobular regions.
131
What are the macroscopic characteristics of a liver affected by steatosis?
Macroscopically, the liver appears very large (4-6 kg or more), soft, yellow, and greasy.
132
Explain the term steatohepatitis.
Steatohepatitis refers to the presence of both inflammation and steatosis in the liver.
133
What is hepatocyte ballooning?
Hepatocyte ballooning is characterized by the swelling and necrosis of single or scattered foci of hepatocytes.
134
Describe Mallory-Denk bodies and their significance in liver pathology.
Mallory-Denk bodies are damaged intermediate filaments seen as eosinophilic inclusion bodies in degenerating hepatocytes, indicating liver injury.
135
What is the role of neutrophils in steatohepatitis?
Neutrophils accumulate around degenerating hepatocytes in steatohepatitis, indicating an inflammatory response.
136
Describe the condition previously known as non-alcoholic fatty liver disease (NAFLD).
Metabolic associated fatty liver disease (MAFLD) refers to liver disease that develops due to obesity and type 2 diabetes mellitus, characterized by the accumulation of fat in the liver without alcohol abuse.
137
Explain the progression of metabolic associated fatty liver disease (MAFLD).
MAFLD progresses similarly to alcoholic liver disease (ALD), moving from steatosis to non-alcoholic steatohepatitis (NASH) and eventually to cirrhosis.
138
Define the term metabolic associated fatty liver disease (MAFLD).
MAFLD is a term proposed in 2020 to better describe liver disease associated with metabolic dysfunction, particularly obesity and type 2 diabetes, replacing the older term NAFLD.
139
How does insulin resistance contribute to MAFLD?
Insulin resistance leads to the accumulation of triglycerides in hepatocytes through impaired oxidation of fatty acids, increased synthesis and uptake of fatty acids, and decreased hepatic secretion of VLDL cholesterol.
140
Explain the impact of oxidative stress on hepatocytes in MAFLD.
Fat-loaded hepatocytes are sensitive to lipid peroxidation products generated by oxidative stress, which can damage mitochondria and plasma membranes, ultimately leading to apoptosis of the hepatocytes.
141
What role do TNF and IL-6 play in MAFLD?
Increased levels of TNF and IL-6, resulting from oxidative stress or release from visceral adipose tissue, contribute to liver damage and inflammation in MAFLD.
142
Describe the commonality of MAFLD in the Western world.
MAFLD is a very common condition in the Western world, often associated with rising rates of obesity and type 2 diabetes.
143
How does the pathology of MAFLD compare to alcoholic liver disease (ALD)?
The pathology and progression of MAFLD are similar to those of ALD, despite the absence of alcohol abuse in MAFLD.
144
Describe the most common hepatic neoplasms.
The most common hepatic neoplasms are neoplastic carcinomas that originate from the colon, lung, or breast.
145
Explain the characteristics of simple liver cysts.
Simple liver cysts may be single or multiple, are usually asymptomatic, and do not require specific management unless they cause symptoms.
146
How can liver cysts be distinguished from solid lesions?
Liver cysts can be easily distinguished from solid lesions on imaging.
147
Define polycystic liver disease and its implications.
Polycystic liver disease is a condition where many cysts form in the liver, potentially replacing a critical mass of functional liver tissue, which can lead to liver failure.
148
What symptoms may arise from hepatomegaly associated with polycystic liver disease?
Hepatomegaly may cause abdominal pain and possibly abdominal distension.
149
Describe focal nodular hyperplasia (FNH) and its characteristics.
Focal nodular hyperplasia (FNH) is a benign lesion consisting of hyperplastic hepatocyte nodules with a characteristic central stellate scar, localized and well-demarcated.
150
Explain the significance of FNH in terms of malignancy and treatment.
FNH is not a true neoplasm, has no malignant potential, is mostly asymptomatic, and is therefore not usually removed.
151
What are echinococcus cysts and how do they form?
Echinococcus cysts, or hydatid cysts, form after consuming something contaminated with echinococcal tapeworm eggs, leading to the development of cysts in the liver.
152
Describe the potential consequences of echinococcus cysts in the liver.
Echinococcus cysts can grow and compress structures in the liver, potentially destroying liver parenchyma, and their rupture can cause anaphylaxis and death.
153
What is the incubation period for echinococcus cysts?
The incubation period for echinococcus cysts can be very long, lasting up to 50 years.
154
What symptoms might patients experience due to echinococcus cysts?
Patients may experience pain in the upper right quadrant and hepatomegaly due to echinococcus cysts.
155
How are echinococcus cysts typically managed when symptomatic?
Surgery is needed to remove echinococcus cysts as soon as possible if they cause symptoms.
156
Describe Echinococcus cysts and their characteristics.
Echinococcus cysts are often solitary but can be multiple, occurring when parasites spread throughout the biliary tree before dying.
157
Explain the primary causes of liver abscesses in Western countries.
In Western countries, liver abscesses are primarily caused by bacteria, specifically referred to as pyogenic liver abscesses.
158
Identify the common causes of liver abscesses in developing countries.
In developing countries, liver abscesses are mostly caused by parasites.
159
How do liver abscesses typically affect the liver's anatomy?
Liver abscesses mostly affect the right lobe of the liver.
160
Define the routes through which bacteria can reach the liver.
Bacteria can reach the liver through ascending infection in the biliary tract, vascular seeding from the GI tract, direct invasion from a nearby source, or penetrating injury.
161
Explain the nature of infections associated with bacterial liver abscesses.
The infection in bacterial liver abscesses is often polymicrobial.
162
List the most common sources of bacterial liver abscesses.
The most common sources include ascending infections from the biliary tract, spreading of bacteria from the GI tract via the portal vein, and systemic bacteraemia (sepsis).
163
Describe the characteristics of bacterial hepatic abscesses.
Bacterial hepatic abscesses can occur alone or as multiple lesions, with sizes ranging from millimeters to many centimeters, exhibiting liquefactive necrosis with neutrophil infiltration.
164
What treatments are necessary for bacterial liver abscesses?
Antibiotics and drainage are needed for the treatment of bacterial liver abscesses.
165
Discuss the mortality rate associated with untreated liver abscesses.
Untreated liver abscesses have a high mortality rate.
166
Define hepatic adenoma and its association with contraceptive use.
Hepatic adenoma is a rare benign tumor of hepatocytes, commonly associated with contraceptive use, making it more prevalent in females.
167
Explain the potential complications of hepatic adenomas.
Hepatic adenomas can rupture or hemorrhage, which may be life-threatening, and they may also undergo malignant transformation into hepatocellular carcinoma.
168
What is the recommended management for hepatic adenomas?
Hepatic adenomas should be surgically removed, and contraception should be stopped.
169
Describe hepatic haemangioma and its prevalence.
Hepatic haemangioma is the most common benign vascular lesion of the liver, associated with contraceptive use and most common in females aged 30 to 50.
170
What are the typical symptoms and management of hepatic haemangiomas?
Hepatic haemangiomas are mostly asymptomatic, have no malignant potential, and are therefore not usually removed.
171
Describe the composition of cavernous angioma.
Cavernous angioma is composed of many endothelium-lined vascular spaces separated by fibrous septa.
172
Explain the significance of bile duct adenoma in diagnosis.
Bile duct adenoma is a rare benign condition that can be confused with malignant tumors, potentially interfering with differential diagnosis.
173
Define hepatocellular carcinoma (HCC).
Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver, primarily affecting older men and often developing in cirrhotic livers.
174
How does the incidence of HCC change over time?
The incidence of hepatocellular carcinoma (HCC) is increasing.
175
List common causes of hepatocellular carcinoma.
Common causes of HCC include chronic HBV or HCV infection, non-alcoholic fatty liver disease, alcoholic liver disease, and aflatoxin.
176
Identify rare causes of hepatocellular carcinoma.
Rare causes of HCC include hepatotoxic drugs like paracetamol, haemochromatosis, autoimmune hepatitis, alpha-1-antitrypsin deficiency, and Wilson's disease.
177
Explain the role of aflatoxin in liver health.
Aflatoxin is a toxin produced by aspergillus fungi that can contaminate food and cause HCC without cirrhosis, primarily in developing countries.
178
Describe the development of HCC in relation to cirrhosis.
HCC develops from a dysplastic nodule in a cirrhotic liver, which is a precancerous lesion that can be visualized on ultrasound.
179
How do hepatitis B and C viruses affect cancer risk?
Both hepatitis B and C viruses increase cancer risk due to chronic inflammation and high cell turnover, although hepatitis B can incorporate HBsAg into the host genome, while hepatitis C cannot.
180
What is a signature mutation associated with aflatoxin?
Aflatoxin causes a characteristic mutation in the p53 gene known as a signature mutation, indicating that the etiology of HCC is likely due to aflatoxin.
181
Describe fibrolamellar HCC.
Fibrolamellar HCC is a very rare form of hepatocellular carcinoma, with only about 200 new cases diagnosed each year, typically developing in young adults without cirrhosis or other risk factors.
182
What screening methods are used for patients at high risk for HCC?
Patients at high risk for HCC, such as those with cirrhosis or chronic hepatitis B, are screened using AFP and ultrasound, followed by CT or MRI if positive.
183
Explain the importance of imaging findings in diagnosing HCC.
Imaging findings from AFP, ultrasound, CT, or MRI are usually sufficient to diagnose HCC, reducing the need for biopsy, which carries a risk of tumor spread.
184
Describe the symptoms of Hepatocellular Carcinoma (HCC) in its early stages.
HCC does not produce significant symptoms until it is at an advanced stage, and any symptoms may be masked by underlying cirrhosis.
185
Explain the prognosis of Hepatocellular Carcinoma (HCC).
HCC has a poor prognosis because it is rarely possible to completely excise the tumor.
186
Define intrahepatic cholangiocellular carcinoma and its prevalence.
Intrahepatic cholangiocellular carcinoma accounts for 10% of cholangiocarcinoma cases and is known to be rare and aggressive.
187
What is Hepatoblastoma and its significance in pediatric oncology?
Hepatoblastoma is a rare childhood tumor that originates in liver precursor tissue and is the most common primary liver tumor in children aged 0 to 3 years.
188
Describe the typical presentation of Hepatoblastoma.
Hepatoblastoma usually presents as an abdominal mass.
189
Identify the characteristics of hepatic angiosarcoma.
Hepatic angiosarcoma is very rare and aggressive, and it is notably associated with exposure to certain toxins.
190
List the toxins associated with hepatic angiosarcoma.
Hepatic angiosarcoma is associated with exposure to vinyl chloride and thorium dioxide.
191
Explain the historical use of vinyl chloride and thorium dioxide.
Vinyl chloride was formerly used in the plastic industry, while thorium dioxide was used as a radiocontrast material.
192
Define cholelithiasis.
Cholelithiasis refers to the presence of gallstones in the gallbladder.
193
Explain the difference between cholelithiasis and choledocholithiasis.
Cholelithiasis refers to gallstones in the gallbladder, while choledocholithiasis refers to gallstones in the common bile duct.
194
Describe the clinical manifestations of gallstone disease.
Gallstone disease includes asymptomatic gallstones, uncomplicated gallstone disease, biliary colic, complicated gallstone disease, acute calculous cholecystitis, cholangitis, gallstone pancreatitis, and gallstone ileus.
195
What is complicated gallstone disease?
Complicated gallstone disease refers to the presence of gallstone-related complications, such as biliary colic, acute calculous cholecystitis, and others.
196
How does uncomplicated gallstone disease present?
Uncomplicated gallstone disease presents with biliary colic without gallstone-related complications.
197
Explain the prevalence of gallstones in the Western population.
Gallstones exist in 10-15% of the Western population, but only 1-4% become symptomatic.
198
Describe the most common type of gallstone.
The most common type of gallstone is the cholesterol stone, which accounts for 80% of all stones in the West.
199
How does bile formation relate to cholesterol elimination?
Bile formation is the only significant pathway for the body to eliminate excess cholesterol, either as free cholesterol or as bile salts.
200
What happens when cholesterol concentration exceeds the solubilization capacity of bile?
When cholesterol concentration exceeds the solubilization capacity of bile, the solution becomes supersaturated, leading to the potential formation of gallstones.
201
Define the nucleation process in gallstone formation.
The nucleation process is when cholesterol precipitates onto a 'nucleus' or starting point, which then grows as more cholesterol accumulates.
202
What role does biliary stasis play in gallstone development?
Biliary stasis is essential for the development of gallstones, as it allows for the accumulation of substances that can lead to stone formation.
203
Describe the composition of most cholesterol stones.
Most cholesterol stones are not purely cholesterol; they commonly also contain bilirubin-calcium salts.
204
What are pigment stones and how do they form?
Pigment stones are comprised of bilirubin-calcium salts and usually occur in association with chronic hemolysis, which increases bilirubin production.
205
How do cholesterol stones and pigment stones differ in appearance and location?
Cholesterol stones are yellowish and arise exclusively in the gallbladder, while pigment stones are black or brownish and may arise anywhere in the biliary tree.
206
Identify the risk factors for cholesterol stones.
The risk factors for cholesterol stones include obesity, rapid weight loss, and certain dietary factors.
207
Describe the 6 Fs associated with gallstones.
The 6 Fs are Fat (obesity), Female, Fertile (multiparity or pregnancy), Forty (above 40 years of age), Fair-skinned (Caucasian), and Family history.
208
Explain the procedure used to remove gallstones.
Gallstones can be removed by a procedure called ERCP, where a tube is led through the upper GI tract into the biliary tree through the ampulla of Vater to visualize and remove stones if necessary.
209
Define biliary colic and its symptoms.
Biliary colic refers to the characteristic pain that occurs when the gallbladder contracts against an outlet obstructed by gallstones, causing intense, dull pain in the right upper quadrant, often accompanied by sweating, nausea, or vomiting.
210
How does cholecystitis relate to gallstones?
Cholecystitis is almost always associated with gallstones, specifically called calculous cholecystitis, which occurs when gallstones obstruct the neck of the gallbladder or the cystic duct, leading to biliary stasis and inflammation.
211
Explain the complications that can arise from gallstones.
Complications of gallstones include biliary colic, cholecystitis, empyema, cholangitis, gallstone pancreatitis, gallstone ileus, fistula formation, and perforation.
212
Describe the characteristics of chronic cholecystitis.
Chronic cholecystitis is characterized by inflammation of the gallbladder due to gallstone blockage, leading to fibrosis of the gallbladder and an increased risk for gallbladder carcinoma.
213
What factors contribute to the development of pigment stones?
Factors contributing to pigment stones include chronic hemolytic anemias, biliary infection, gastrointestinal disorders, Crohn disease, ileal resection, and cystic fibrosis with pancreatic insufficiency.
214
How does gallbladder obstruction lead to inflammation?
Gallbladder obstruction by gallstones causes biliary stasis, but inflammation requires an additional unknown irritant to contribute to the inflammatory process.
215
What is the typical location of pain associated with biliary colic?
The pain associated with biliary colic is typically located in the right upper quadrant.
216
Do all individuals with gallstones experience symptoms?
No, only a minority of people with gallstones are symptomatic.
217
Describe the primary treatment for cholecystitis.
The primary treatment for cholecystitis is cholecystectomy.
218
Explain the potential complication of bile stasis in cholecystitis.
Bacterial superinfection may occur in case of bile stasis, causing the gallbladder to fill with pus and leading to empyema.
219
Define cholangitis and its common cause.
Cholangitis, also known as ascending cholangitis, refers to inflammation of the biliary tract due to bile stasis caused by choledocholithiasis, which leads to superinfection.
220
What are the classic symptoms of cholangitis as described by Charcot’s triad?
Charcot’s triad includes fever, abdominal pain, and jaundice.
221
How is cholangitis typically managed?
Cholangitis is managed with antibiotics and biliary drainage.
222
Describe the condition that can arise from gallstones obstructing bile flow.
Gallstones that obstruct the flow of bile can cause reflux of bile into the pancreas, leading to gallstone pancreatitis.
223
Identify the location where the offending stone is often found in gallstone pancreatitis.
The offending stone is often found in the ampulla of Vater.
224
What is the management approach for gallstone pancreatitis?
Gallstone pancreatitis is managed with Endoscopic Retrograde Cholangiopancreatography (ERCP).
225
Define cholangiocellular carcinoma (CCC).
Cholangiocellular carcinoma, also known as cholangiocarcinoma, is a malignancy of the cholangiocytes that line the bile ducts.
226
Differentiate between extrahepatic and intrahepatic cholangiocellular carcinoma.
Extrahepatic cholangiocellular carcinoma causes obstruction of the bile ducts quickly, leading to early diagnosis, while intrahepatic types are often discovered late, resulting in a worse prognosis.
227
What is a Klatskin tumor?
A Klatskin tumor occurs at the confluence of the right and left hepatic bile ducts.
228
Discuss the prevalence and demographic affected by cholangiocarcinoma.
Cholangiocarcinoma is a rare cancer that mostly affects elderly men.
229
What is the typical treatment for cholangiocarcinoma?
The treatment for cholangiocarcinoma is surgical, but more than 90% of cases are unresectable at the time of diagnosis, making them incurable.
230
List some risk factors associated with cholangiocarcinoma.
Risk factors for cholangiocarcinoma include cirrhosis, choledocholithiasis, and primary sclerosing cholangitis.
231
Explain how gallbladder cancer develops.
Gallbladder cancer arises from the gallbladder mucosa and may develop from gallbladder polyps.
232
What is the common symptomatology of gallbladder cancer in its early stages?
Gallbladder cancer is often asymptomatic in the early stages and is frequently diagnosed incidentally after a cholecystectomy for gallstones.
233
Identify the most common cause of gallbladder cancer.
The most common cause of gallbladder cancer is chronic cholecystitis due to cholelithiasis.
234
Describe the composition of the exocrine pancreas.
The exocrine pancreas is composed of ductules, ducts, and acinar cells that produce digestive enzymes.
235
Explain the function of zymogen granules in the pancreas.
Zymogen granules store digestive enzymes in their inactive pro-enzyme form to prevent activation before reaching the duodenum.
236
Define acute pancreatitis.
Acute pancreatitis is a reversible inflammatory condition of the pancreas that can range from mild edema to severe parenchymal necrosis.
237
How does trypsinogen convert to trypsin in the pancreas?
Trypsinogen is converted to trypsin by duodenal enteropeptidase, which activates the digestive enzymes.
238
What mechanisms prevent premature activation of digestive enzymes in the pancreas?
The pancreas prevents premature activation by synthesizing enzymes as inactive proenzymes, secreting trypsin inhibitors, and having acinar cells resistant to activated enzymes.
239
Explain the term autodigestion in relation to the pancreas.
Autodigestion of the pancreas occurs when digestive enzymes are prematurely activated within the pancreas, leading to self-digestion and pancreatitis.
240
List the common causes of acute pancreatitis.
The most common causes of acute pancreatitis are alcoholism and gallstones, which account for 80% of all cases.
241
What is the significance of the acronym GET SMASHED in the context of pancreatitis?
GET SMASHED is an acronym that summarizes the common causes of acute pancreatitis: Gallstones, Ethanol, Trauma, Steroids, Mumps virus, Autoimmune conditions, Scorpion venom, Hypercalcemia, Hyperlipidemia, ERCP, and Drugs.
242
Describe the mortality rate associated with acute pancreatitis.
The mortality rate for acute pancreatitis is around 5%, but it can be higher in cases of severe necrotizing pancreatitis with complications.
243
How does trypsin function as a negative feedback mechanism in the pancreas?
Trypsin cleaves and inactivates itself, serving as a negative feedback mechanism to prevent excessive activation of digestive enzymes.
244
What are the potential complications of severe acute pancreatitis?
Severe acute pancreatitis can lead to complications such as organ failure and has a high mortality rate.
245
Identify other causes of acute pancreatitis beyond the common ones.
Other causes of acute pancreatitis include vascular issues, mutations (like PRSS1 and SPINK1), and idiopathic factors.
246
Describe the effect of alcohol on pancreatic juice viscosity and the sphincter of Oddi.
Alcohol increases the viscosity of pancreatic juice and increases the tone of the sphincter of Oddi, which decreases the outflow of pancreatic juice.
247
Explain the consequences of decreased outflow of pancreatic juice due to gallstones.
Decreased outflow of pancreatic juice due to gallstones can lead to the activation of digestive enzymes inside the pancreas, resulting in tissue damage and necrosis.
248
How does elastase contribute to pancreatic damage during acute pancreatitis?
Elastase digests the vasculature, causing fluid leakage into the parenchyma, leading to edema and further damage to blood vessels.
249
Define adiponecrosis in the context of acute pancreatitis.
Adiponecrosis is the process where pancreatic lipases digest triacylglycerols in adipocytes, forming free fatty acids that combine with calcium to create soap.
250
What are the basic alterations observed in acute pancreatitis?
The basic alterations in acute pancreatitis include microvascular leakage causing edema, proteolytic destruction of pancreatic parenchyma, adiponecrosis, acute inflammatory reaction, and interstitial hemorrhage.
251
Distinguish between the two forms of acute pancreatitis.
The two forms of acute pancreatitis are oedematous type, which accounts for 80% of cases and is milder, and necrotising/haemorrhagic type, which accounts for 20% of cases and is more severe.
252
Explain the histological features of oedematous acute pancreatitis.
Histological features of oedematous acute pancreatitis include interstitial edema, inflammatory cell infiltrate, and adiponecrosis, but no hemorrhage or interstitial necrosis.
253
What is the mortality rate associated with oedematous acute pancreatitis?
Oedematous acute pancreatitis has an almost zero percent mortality rate.
254
Describe the histological features of necrotising or haemorrhagic acute pancreatitis.
Histological features of necrotising or haemorrhagic acute pancreatitis include patchy necrosis, interstitial edema, adiponecrosis, inflammatory cell infiltrate, and interstitial hemorrhage.
255
How can necrosis in necrotising acute pancreatitis affect prognosis?
Necrosis in necrotising acute pancreatitis may become infected, which worsens the prognosis.
256
What are the early complications of oedematous acute pancreatitis?
Early complications of oedematous acute pancreatitis include acute peripancreatic fluid collections, which are non-encapsulated and do not contain necrosis.
257
Define pseudocysts in the context of late complications of oedematous acute pancreatitis.
Pseudocysts are late complications formed when liquefied areas of necrotic pancreatic tissue become walled off by fibrous tissue.
258
Describe the treatment approach for chronic pancreatitis.
Treatment is mostly supportive, focusing on fluid administration to prevent shock and denying oral feeding to avoid stimulating pancreatic secretions.
259
Explain the characteristics of chronic pancreatitis.
Chronic pancreatitis is characterized by chronic inflammation of the pancreas, leading to the replacement of normal parenchyma with fibrotic scar tissue, resulting in chronic abdominal pain and pancreatic insufficiency.
260
Define the TIGAR-O system in relation to chronic pancreatitis.
The TIGAR-O system classifies the causes of chronic pancreatitis into Toxic-metabolic factors, Idiopathic, Genetic, Autoimmune, Recurring acute pancreatitis, Obstructive chronic pancreatitis.
261
List the toxic-metabolic factors associated with chronic pancreatitis.
The toxic-metabolic factors include alcohol abuse, tobacco smoking, and hypertriglyceridaemia.
262
How does chronic pancreatitis affect pancreatic function?
Chronic pancreatitis can lead to chronic malabsorption and steatorrhoea due to loss of exocrine function, and diabetes mellitus due to loss of endocrine function.
263
Describe the common symptoms of chronic pancreatitis.
The most common symptoms include epigastric abdominal pain radiating to the back and nausea/vomiting.
264
Explain the types of neoplasms that can originate from the pancreas.
Neoplasms of the pancreas can originate from endocrine cells (endocrine tumours) or exocrine cells (exocrine tumours), which may be cystic or solid.
265
What are the types of cystic neoplasms of the pancreas?
Cystic neoplasms include serous cystadenomas, mucinous cystadenomas, and intraductal papillary mucinous neoplasms.
266
Identify the solid neoplasms associated with the pancreas.
Solid neoplasms include solid pseudopapillary neoplasm/solid papillary cystic neoplasia and pancreatic adenocarcinoma.
267
Discuss the complications that may arise from chronic pancreatitis.
Complications of chronic pancreatitis include chronic malabsorption, steatorrhoea, and diabetes mellitus.
268
What is the significance of pancreatic adenocarcinoma in relation to pancreatic neoplasms?
Pancreatic adenocarcinoma is one of the most lethal malignancies among pancreatic neoplasms.
269
Describe pancreatic adenocarcinoma and its common characteristics.
Pancreatic adenocarcinoma, commonly known as pancreatic cancer, is an aggressive cancer with a high mortality rate. It typically presents no early symptoms, making it difficult to treat, and primarily affects elderly individuals aged 60 to 80.
270
Explain the common risk factors associated with pancreatic adenocarcinoma.
Common risk factors for pancreatic adenocarcinoma include smoking, chronic pancreatitis, alcoholism, and obesity.
271
Define the types of pancreatic cancer and their origins.
Pancreatic cancer primarily consists of pancreatic adenocarcinoma, which accounts for almost all malignant exocrine pancreatic cancers. It originates from the epithelial cells of the pancreatic tubules.
272
How are pancreatic adenocarcinoma cases distributed within the pancreas?
Approximately 60% of pancreatic adenocarcinoma cases are located in the head of the pancreas, while the remaining 40% are evenly distributed throughout the body and tail.
273
Explain the prognosis for tumors located in the head of the pancreas compared to those in the body and tail.
Tumors located in the head of the pancreas have a better prognosis because they cause symptoms earlier, leading to earlier diagnosis. In contrast, tumors in the body and tail produce symptoms later, often resulting in late-stage diagnosis.
274
List common symptoms of pancreatic adenocarcinoma.
Common symptoms include belt-shaped epigastric pain, posthepatic (obstructive) jaundice, Courvoisier’s sign (enlarged but nontender gallbladder), and Trousseau’s sign (recurring migratory thrombophlebitis).
275
Describe the aggressiveness of pancreatic adenocarcinoma and its implications for treatment.
Pancreatic adenocarcinoma is very aggressive, often presenting with metastases at diagnosis. It frequently invades local structures, making many cases inoperable.
276
What is the 5-year survival rate for pancreatic adenocarcinoma?
The 5-year survival rate for pancreatic adenocarcinoma is less than 5%.
277
Define pancreatic endocrine tumors and their origin.
Pancreatic endocrine tumors are neuroendocrine tumors that produce hormones and originate from the Langerhans islet cells. They account for less than 5% of pancreatic tumors.
278
Explain the potential malignancy of pancreatic endocrine tumors.
Pancreatic endocrine tumors are predominantly benign but can be malignant. Their disruptive potential mainly arises from their hormone-producing properties rather than their mass effect or invasion.
279
What are some types of pancreatic endocrine tumors and their associated hormones?
Types of pancreatic endocrine tumors include insulinoma (produces insulin), gastrinoma (produces gastrin), VIPoma (produces vasoactive intestinal peptide), glucagonoma (produces glucagon), and somatostatinoma (produces somatostatin).
280
Describe the clinical effects of insulinomas and gastrinomas.
Insulinomas cause hypoglycemia, while gastrinomas lead to severe peptic ulcer disease.
281
What is the association between some endocrine pancreatic tumors and multiple endocrine neoplasia (MEN) type 1?
A few percent of endocrine pancreatic tumors are associated with multiple endocrine neoplasia (MEN) type 1.
282
Describe serous cystadenomas and their characteristics.
Serous cystadenomas are the most common cystic neoplasm of the pancreas, occurring most frequently in older female patients. They are almost always benign and are associated with mutations in the VHL tumor suppressor gene.
283
Explain the significance of mucinous cystadenomas in pancreatic tumors.
Mucinous cystadenomas are almost exclusively found in women and are usually located in the body or tail of the pancreas. They are filled with thick mucin, and up to one third of these neoplasms can have dysplasia, which increases the risk of becoming malignant.
284
How do intraductal papillary mucinous neoplasms (IPMN) differ in prevalence between genders?
Intraductal papillary mucinous neoplasms (IPMN) are more common in males than in females.
285
Define the potential for malignancy in intraductal papillary mucinous neoplasms.
Up to two thirds of intraductal papillary mucinous neoplasms (IPMN) have mutations that increase their potential to turn malignant.
286
What is the typical demographic affected by solid pseudopapillary neoplasms?
Solid pseudopapillary neoplasms typically affect mainly young females.
287
Describe the behavior of solid pseudopapillary neoplasms.
Solid pseudopapillary neoplasms are locally aggressive tumors with low malignant potential, and they do not metastasize.
288
Explain the general importance of benign pancreatic tumors in medical knowledge.
Benign pancreatic tumors are rare and not considered critically important to know in the broader context of pancreatic pathology.
289
How are serous cystadenomas associated with genetic mutations?
Serous cystadenomas are associated with mutations in the VHL tumor suppressor gene.
290
Identify the common locations for mucinous cystadenomas in the pancreas.
Mucinous cystadenomas are usually found in the body or tail of the pancreas.
291
Discuss the risk factors associated with mucinous cystadenomas.
Mucinous cystadenomas have a risk factor of dysplasia, with up to one third of these neoplasms potentially becoming malignant.
