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Robbins Pathology GI (Chptr 16,17,18,19) > Chapter 18-Liver > Flashcards

Chapter 18-Liver Flashcards

1
Q

What is the main blood supply for the liver

A

The portal vein provides 60-70% of blood flow

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2
Q

What are the three components of the portal triad

A
  • Portal veins
  • Hepatic arteries
  • Bile ducts
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3
Q

Ischemic and hypoxic events are most likely to affect which zone of the hepatic lobule

A

Zone 1

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4
Q

Drugs and toxins in the liver are most likely to damage which lobular zone

A

3

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5
Q

What are the main primary diseases of the liver

A
  • Viral hepatitis
  • NAFLD
  • Alcoholic liver disease
  • hepatocellular carcinoma
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6
Q

What are the cytosolic serum measurements that can be ordered to investigate the integrity of the liver

A

AST
ALT
Lactate dehydrogenase (LDH)

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7
Q

What is the serum measurement that can be take for testing the biliary excretory function

A
  • Serum bilirubin
  • Urine bilirubin
  • Serum bile acids
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8
Q

What is direct serum bilirubin looking at

A

The amount of conjugated bilirubin

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9
Q

Which tests can be ordered to evaluate the love of damage to the bile canaliculus

A

Serum alkaline phosphatase

Serum gamma-glutamic transpeptidase (GGT)

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10
Q

Which serum level can be used to test for the amount of hepatic demethylation

A

Aminopyrine breath test

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11
Q

What are the two major hepatic changes that are reversible

A

Steatosis and cholestasis

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12
Q

What is the process and condition if there are councilman bodies or acidophil bodies present

A

Hepatic apoptosis

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13
Q

What is confluent necrosis and where does it normally begin

A

Widespread necrosis where there is zonal loss due to toxic or ischemic events, usually starting around a central vein

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14
Q

What is a bridging necrosis event

A

Zone of necrosis that links central veins to portal tracts or bridges them

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15
Q

IN the regeneration of the liver, which cytokines are present in the priming phase

A

TNF and IL6

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16
Q

IN the regeneration of the liver, which cytokines are present in the growth phase

A

HGF and TGF-alpha

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17
Q

What is the principal cell involved in the hepatic scar deposition

A

Hepatic stellate cell

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18
Q

What is the function of the stellate cell in a quiescent form

A

Lipid Vitamin A storage

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19
Q

What does the stellate cell become in the phase of hepatic repair

A

Highly fibrotic myofibroblasts

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20
Q

What is the process that initiates the stellate cells to become myofibroblasts

A
  • Increased production of platelet derived growth factor Beta receptor (PDGFR-Beta) in the stellate cells
  • Increased production of TGF-Beta and receptors
  • increased metalloproteinase 2 (MMP2)
  • Increased tissue inhibators of metalloproteinase 1 and 2 inhibators (TIMP2)
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21
Q

Once stellate cells become myofibroblasts, what is their function

A

Are contractile cells and are activated by endothelin-1 (ET-1)

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22
Q

What percentage of the liver functional capacity must be affected to cause hepatic failure

A

80 to 90%

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23
Q

What defines a case of acute hepatic liver failure

A

Acute liver illness with encephalopathy and coagulation that occurs 26 weeks after an initial liver injury, and must in the absence of pre-existing liver disease

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24
Q

What is the most common cause of acute liver failure

A

Massive hepatic necrosis, most often induced by drugs or toxins

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25
Q

Ingestion of which toxic is the most common cause of acute liver toxicity

A

50% occur due to ingestion (accidental or purposefully) of acetaminophen

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26
Q

IN Asia, what is the most common cause of acute liver toxicity

A

Hepatitis B and E

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27
Q

What is the time frame that acetaminophen causes liver toxicity

A

Within a week

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28
Q

IN the case of direct liver toxicity like with acetaminophen, what is the size and characteristic of the liver

A

Small and shrunken, without signs of scarring or regeneration due to the quick nature of the toxicity and failure.

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29
Q

What are the feature of the liver when damage is caused by viral infection

A

Failure is due to weeks or months of injury, so while the attack is acute, it will still show signs of regeneration and scarring

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30
Q

What are the conditions that can cause poisoning of the liver cells without any evidence of cell death and parenchymal collapse

A

Diffuse microvascular steatosis related to fatty liver of pregnancy and reactions to toxins

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31
Q

Which toxins can cause diffuse microvascular steatosis

A

Valproate and tetracycline

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32
Q

What is the general clinical presentation of acute liver failure

A
  • Nausea, vomiting, and jaundice

- Followed by encephalopathy and coagulation defects

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33
Q

Cholestasis increases the risk of which condition

A

Life threatening bacterial infections

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34
Q

Hepatic encephalopathy is characterized by what presentations

A
  • Confusion, stupor, coma or death
  • Rigidity and hyperreflexia
  • asterixis (rapid extension/flexion of the head and extremities)
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35
Q

How will Asterixis present and is characteristic of which condition

A

Rapid flexion/extension of the head and extremities, best seen with arms are in extension and wrists are dorsiflexed.
-Indicative of hepatic encephalopathy

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36
Q

The encephalopathies seen in hepatic failure are due to abnormal levels of what in the serum

A

Ammonia leading to neural dysfunction

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37
Q

What is the relation between hepatic failure and coagulation issues

A

Liver produces vitamin K dependent and independent clotting factors, so impaired hepatic function decreases, there is a decrease in the ability to clot, along with the development of DIC

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38
Q

What is hepatorenal syndrome defined as

A

Renal failure that is occurring in patients with hepatic failure, with no appearance or reason for kidney failure

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39
Q

What is the result of hepatorenal function on the serum concentrations

A

Decreased GFR and renal perfusion pressure due to:

  • Systemic vasodilation
  • activation of SNS
  • Increased renin/angiotensin axis
  • Increased renal vasoconstriction
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40
Q

What is chronic liver failure most associated with and what is the morphology of the result

A

Liver cirrhosis, characterized by regenerative parenchymal nodules surrounded by fibrous bands and vascularization

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41
Q

How do cirrohosis livers appearances during a biopsy tend to not develop portal hypertension

A

-narrow, dense, and compacted septa which are separated by large islands of intact parenchyma

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42
Q

How do cirrohosis livers appearances during a biopsy tend develop portal hypertension

A

-Broad bands of dense scarring, with dilated lymphatic spaces, with less intervening healthy parenchyma

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43
Q

How will patients with cirrhosis present in the clinic

A

Anorexia, weight loss, weakness

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44
Q

What are the normal causes of fatality in those patients with cirrhosis

A
  • Hepatic encephalopathy
  • Bleeding of esophageal varicose veins
  • Bacterial infections
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45
Q

During chronic liver injury, even if the cause is removed, which risks factors still remain

A
  • Portal hypertension due to formation of irreversible shunts
  • Hepatocellular carcinoma
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46
Q

What are common effects seen in chronic liver failure with regards to hormones and their result

A

Impaired estrogen metabolism, leading to hyperestrogenemia:

  • palmar erythema (local vasodilation)
  • spider angiomas
  • hypogonadism and gynocomastia
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47
Q

What are the common causes of prehepatic conditions leading to portal hypertension

A

Obstructive thrombosis
Narrowing of the portal vein
Increased splenic venous blood flow

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48
Q

What are the common causes of posthepatic conditions that lead to portal hypertension

A

Right sided heart failure
Constructive pericarditis
Hepatic vein outflow obstruction

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49
Q

What is the main cause of intrahepatic conditions leading to portal hypertension

A

Cirrhosis

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50
Q

What is the leading cause of hepatic hypertension

A

Cirrhosis

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51
Q

Alteration in sinusoidal endothelial cells contribute to intrahepatic vasoconstriction and Portal Hypertension through which chemicals

A
  • Decrease in NO
  • Increased endothelin-1 (ET-1)
  • Angiotensinogen
  • Eicosanoid
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52
Q

What is the correlation between splanchnic circulation changes and portal hypertension

A
  • Increased portal venous blood flow from hyperdynamic circulation caused by vasodilation in the Splanchnic circulation
  • Overall leads to increased venous efflux
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53
Q

What is the most common cause of ascites

A

Cirrhosis

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54
Q

In the case of patients with ascites, what does the presence of neutrophils in the fluid mean

A

Infection

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55
Q

In the case of patients with ascites, what does the presence of blood in the fluid point to

A

Disseminated intra-abdominal cancer

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56
Q

With long standing ascities, what is the process of hydrothroax and which side is it more common on

A

-Seepage of peritoneal fluid through trans-diaphragmatic lymphatics, usually on the right side

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57
Q

What are the three mechanism that can lead to ascites pathogenesis

A

1-sinusiodal hypertension
2-percolation of hepatic lymph into the peritoneal cavity
3-Splanchnic vasodilation and hyperdynamic circulation

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58
Q

What is happening in the sinusoidal hypertension as a result of ascities pathogensis

A

Alterations in Starling’s forces, which drive fluid into space of Disse (also promoted by hypoalbumininemia), where it is removed by hepatic lymphatics

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59
Q

What is the happening in the percolation of hepatic lymph into the peritoneal cavity as a result of portal hypertension and formation of ascites

A

With cirrhosis, normal lymph flow is far exceeding what is normally does, so there is more than the thoracic duct can handle. As a result, protein rich and triglyceride poor fluid accumulates as part of the ascites fluid

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60
Q

In the case of patients with ascites, what does the presence of splanchnic vasodilation and hyper-dynamic circulation as a result of portal hypertension that results in ascites

A

Arterial vasodilation in the splanchnic circulation and reduces that arterial blood pressure. The CO is unable to compensate and as a result vasoconstrictors are activated,leading to excess fluid leaving into the abdominal cavity

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61
Q

What is the result on the spleen as a result of liver congestion

A

Splenomegaly, leading to hypersplenism, such as thrombocytopenia and pancytopenia

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62
Q

What is hepatopulmonary syndrome and what is a common cause

A

Seen in 30% of patients with cirrhosis and portal hypertension:
-When the intrapulmonary vasculature dilates, including capillaries, resulting in hypoxia

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63
Q

What is mechanism of hepatopulmonary syndrome

A

-Intrapulmomsry vasculature, including capillaries, dilate. This results in ventilation/perfusion mismatch and hypoxia, creates and right to left shunt

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64
Q

What position that exacerbates hepatopulmonary syndrome

A

Dyspnea in the upright position

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65
Q

What are the clinical findings of portopulmonary hypertension and what is the common cause

A

Caused by liver disease and portal hypertension, leading to vasoconstriction and vascular remodeling of the pulmonary arteries
-dyspnea upon exertion and clubbing of the fingers

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66
Q

What is a cause of acute on chronic liver failure with regards to hepatitis origin

A

-Chronic Hepatitis B infection in a patients who become infected with hepatitis D

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67
Q

What is the cause of acute on chronic liver failure with regards to ascending cholagitis

A

Ascending cholagitis in a patients with primary sclerosing cholagitis is fibropolycystic liver disease

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68
Q

Overall, what is the very general mechanism of acute on chronic liver disease

A

-A well compensated chronic liver disease undergoes distress when an acute and new toxin/event causes changes that the remaining parenchyma can not handle

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69
Q

What is the usually clinical course and outcome of Hepatitis A infection

A

Usually benign, self limited disease with 2-6 weeks of incubation period

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70
Q

What are the common locations that Hepatitis A infections are occuring

A

Places with poor hygiene and sanitation with a fecal oral transmission

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71
Q

Which marker is a reliable indication for an acute hepatitis A infection

A

Anti HAV IgM titer, as a rise in this also indicates lack of fecal shedding

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72
Q

What are the five potential outcomes from a hepatitis B infection

A

1-Acute hepatitis with recovery and clearance
2-nonprogressive chronic hepatitis
3-progressive chronic disease with cirrhosis
4-acute hepatic failure with massive liver necrosis
5-asympatmatic healthy carrier

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73
Q

Which cancer is hepatitis B an important precursor for

A

Hepatocellular carcinoma (even in the absence of cirrhosis)

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74
Q

The carrier rate for hepatitis B is largely determined by which factor

A

The age of infection, as infection in children leads to a higher carrier rate

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75
Q

What is the main transmission route for hepatitis B

A

90% is due to transmission during childbirth

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76
Q

In areas of low levels of Hepatitis B prevalence, what is the most common route of transmission

A

Sexual contact or drug use

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77
Q

How are most hepatitis B infections prevented

A

Use of the vaccine as it is 95% successful

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78
Q

What is the location of hepatitis B during active and chronic infections

A

In the Blood

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79
Q

What percentage of patients with chronic hepatitis due to hepatitis B recover

A

1-2% of the patients spontaneously clear the infection

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80
Q

What is the result of most patients with an acute or subclinical disease

A

Recovery

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81
Q

What is the result of the majority of patients who develop chronic hepatitis

A

Cirrhosis

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82
Q

What is the function of the hepatitis B preform region

A

Directs the secretion of the core region aka HBeAg

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83
Q

What is the activity of the Pol portion of hepatitis B

A

A polymerase that is a DNA polymerase and reverse transcriptase

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84
Q

What portion of the hepatitis B virus has been indicated in cancer and which cancer is it

A

HBx (activates transcription) in hepatocellular carcinoma

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85
Q

What are the levels of HBsAg over the course of a hepatitis B infection

A

HBsAg:

  • Appears before onset of symptoms
  • Peaks during disease
  • Undetectable by week 12
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86
Q

What are the levels of anti-HBs antibody over the course of a hepatitis B infection

A

Anti-HB antibodies:

  • Rises after acute distress
  • Usually after the disappearance of HBsAg
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87
Q

What are the levels of HBeAg, HBV-DNA, and DNA polymerase over the course of a hepatitis B infection

A

Appear in serum after HBsAg, and present during viral replication

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88
Q

What marker is the HBeAg used to monitor

A

Continues viral replication, infectivity, and progression to chronic hepatitis

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89
Q

What does the presence of anti-HBe antibodies imply

A

Acute infection has peaked and is winding down

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90
Q

What is the main determinant of the result of a hepatitis B viral infection

A

Host immune response

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91
Q

During the hepatitis B infection, what is causing the destruction to the liver

A

CD8 T cells

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92
Q

What is the best predictor of chronicity of hepatitis B infection

A

Age (the younger at onset, more likely to develop)

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93
Q

What are the common risk factors for hepatitis C

A
  • IV drug users (54%)
  • Sexual partners (36%)
  • Surgury in last 6 months (16%)
  • Needle stick (10%)
  • Contact with infected with HCV (10%)
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94
Q

What is the target of the hepatitis C antibodies and what is the characteristic of that target

A

-E2 protein is the target, but serves to be the most variable portion of the virus

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95
Q

Why is there no vaccine to hepatitis C

A

-Genomic instability and antigenic variability as even the presence of IgG does not incur lifelong immunity

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96
Q

What is a typical feature of the clinical infection course of disease for hepatitis C

A

-Repeated bouts of hepatic damange due to the reactivation of preexisting infection or the emergence of an endogenous, new strain

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97
Q

Which condition is very commonly associated with hepatitis C infected patients

A

Chronic disease in (80-90%), resulting in cirrhosis in 20% of them

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98
Q

In those patients with chronic hepatitis, which test should be run for diagnosis and what is it evaluating

A

Hepatitis C RNA testing for assessment of viral replication and conformation of diagnosis

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99
Q

In patients with chronic hepatitis C viral infection, what is a characteristic serum finding

A

Persistent elevations in serum aminotransferases

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100
Q

Which syndrome is highly associated with hepatitis C infection

A

Metabolic syndrome, as it can cause insulin resistance and NAFLD, particularly with genotype 3

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101
Q

Treatment of hepatitis C infection with what can possibly provide a cure

A

Pegylated IFN

Ribavirin

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102
Q

Patients with which hepatitis C genotype are generally likely to have a better response to treatment

A

2 or 3

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103
Q

Which polymorphism can result in better responses to hepatitis C treatment

A

Polymorphism in the IL28B gene

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104
Q

What is the general clinical outcome in a patient who is infected with a co-infection of the Hepatitis B and D

A

Usually self limiting and there is clearance of both viruses in healthy non-IV drug users

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105
Q

Which population is at a higher risk of acute hepatic failure when co-infected with hepatitis B and D

A

IV drug users

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106
Q

What is the result in patients who are infected with chronic hepatitis B and are inoculated with hepatitis D

A

Superinfection, resulting in chronic hepatitis D in almost all patients

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107
Q

What is the most reliable indicator of hepatitis D viral infection

A

IgM anti-HDV antibodies

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108
Q

What is the route of infection of hepatitis E and what is the common patient population affected

A

Zoonotic disease (pigs) that is a water Bourne infection primarily occurring in young to middle aged adults

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109
Q

Which patients are at an increased risk of poor prognosis as a result of infection with hepatitis E

A

Pregnant women as mortality is 20%

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110
Q

What is the relationship between hepatitis E and immunocompetent patients with regards to chronic conditions

A

Does not cause chronic liver disease or persistence of viremia

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111
Q

What are the clinical features of hepatitis infections with acute asymptomatic infection with recovery

A
  • Subclinical and only found accidental

- Minimally elevated serum transaminases

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112
Q

What are the clinical features of hepatitis infections with scute symptomatic infection with recovery

A

1) Incubation period
2) symptomatic preicteric phase
3) symptomatic icteric phase
4) Convalescence

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113
Q

What are the clinical features of hepatitis infections with acute liver failure

A

Hepatitis A and E are most common causes

-activation of stem cells from canal of Hering, no other real symptoms/treatments other than supportive

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114
Q

What are the clinical features of hepatitis infections with chronic hepatitis

A

All Changes continuing or relapsing diseases for longer than 6 months:

  • Elevations in transaminases
  • prolonged prothrombin time
  • fatigue
  • hepatomegaly, hepatic tenderness and mild splenomegaly
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115
Q

Which condition is commonly found to have cyroglobulemia

A

Chronic hepatitis C infection (in 35% of patients)

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116
Q

What percentage of patients with an acute hepatitis C viral infection with progress to a chronic hepatitis

A

80%

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117
Q

The presence of spotty necrosis or lobular hepatitis are indicative of which kind of injury

A

Acute viral hepatitis

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118
Q

In severe acute hepatitis, where is the damage seen and what are the common histological findings

A

Occurs around the central veins and accompanying severity are central-portal bridging necrosis, along with even worse parenchymal collapse

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119
Q

What is the characteristic histological feature of chronic viral hepatitis

A

Mononuclear portal infiltration

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120
Q

What condition is found to have interface between the hepatocellular parenchyma and portal tract stroma, along with scarring

A

Progressive chronic hepatitis

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121
Q

What is the histological progression of chronic hepatitis infection histologically

A
  • Only the portal ducts exhibit fibrosis at first

- Over time, there is increasing ductular reaction, which reflects the stem cell action

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122
Q

Which condition is characterized by histological feature of ground glass hepatocytes

A

Hepatitis B, caused by ER swelling by HBsAg

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123
Q

Which condition shows lymphoid aggregates or fully formed lymphoid follicles, commonly with fatty changes

A

Hepatitis C

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124
Q

Which parasite is the common cause of cholangiocarcinoma in Southeast Asia

A

Liver flukes

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125
Q

What are hydatid cysts caused by and what is usually used to confirm the diagnosis

A

Caused by echinococcal infections and are confirmed by their calcification in the cyst walls

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126
Q

Autoimmune hepatitis is commonly associated with which HLA

A

DRB1 alleles

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127
Q

What are the common patient populations seen to have autoimmune hepatitis

A

White females

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128
Q

Which autoimmune hepatitis is known to affect middle aged to older individuals

A

Type 1

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129
Q

Which autoimmune hepatitis is known to affect individuals in their teens and children

A

Type 2

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130
Q

Type 2 autoimmune hepatitis are known have antibodies against which antigens

A
  • antinuclear (ANA)
  • antismooth muscle actin (SMA)
  • anti-soluble liver antigen/liver-pancreas (SLA/LP)
  • anti-mitochondrial (AMA)
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131
Q

Type 1 autoimmune hepatitis are known have antibodies against which antigens

A
  • Anti-liver Kidney microsomes 1(LKM-1)
  • Anti-CYP2D6
  • Anti-liver cytosol-1 (ACL-1)
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132
Q

How is autoimmune hepatitis distinguished from viral hepatitis

A

The time frame, as viral hepatitis is a slower longer period of destruction and subsequent scarring. Autoimmune hepatitis is rapid damage, followed by rapid scarring

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133
Q

Which condition is characterized histologically by plasma cell predominance in inflammatory infiltrates and “rosettes” in ares of activity

A

Autoimmune hepatitis

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134
Q

How would acute hepatic damage be differentiated as the origin from drug toxicity or autoimmune hepatitis

A

Both will have little/no scarring:
Autoimmune hepatitis- Confluent necrosis
Drug toxicity- Lobule necrosis

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135
Q

Which patient population tends to have a better prognosis with regards to autoimmune hepatitis

A

Adults over children

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136
Q

What is the result of liver transplantation in patients with autoimmune hepatitis

A

-High 10 year survival, but there is a 20% chance of recurrence

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137
Q

What conditions are autoimmune gastritis associated with

A

Autoimmune conditions, particularly primary biliary cirrhosis (more common) or primary sclerosing cholangitis

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138
Q

What is the most common agent the produces toxic liver injury

A

Alcohol

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139
Q

What is the manner in which predictable reactions affect all people

A

Dose dependent manner

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140
Q

What is the most common toxins causing acute hepatic failure and the need for a liver transplant

A

Acetaminophen

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141
Q

What aspect of acetaminophen is toxic and where is it formed

A

CYP450 in the liver creates a toxic byproduct

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142
Q

What are two examples of idiosyncratic reactions that cause liver damage

A
  • chlorpromazine

- halothane

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143
Q

What is the leading cause of liver disease in most western countries

A

Excessive alcohol consumption

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144
Q

What are the three distinctive forms of alcoholic liver injury

A

1-Hepatocellular steatosis or fatty change
2-Alcoholic hepatitis
3-Steatofibrosis

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145
Q

What are the morphological findings in hepatic steatosis (fatty liver)

A

-Lipid begins as small droplets that coalesce into large droplets which distend the hepatocytes and push the nucleus aside, but is completely reversible

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146
Q

What does the presence of hepatocytes swelling and necrosis, Mallory Denk bodies, and Neutrophilic reactions signify

A

Alcoholic (steato-) hepatitis

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147
Q

What is the histological findings of the hepatocytes swelling and necrosis that is seen in alcoholic hepatitis

A

Ballooning of cells and necrosis due to the accumulation of fat and water

148
Q

What is the histological findings of Mallory-Denk bodies

A

Clumped, amorphous, eosinophilia material in ballooned hepatocytes, leaving almost an “empty” cytoplasm
-characteristic of alcoholic liver disease

149
Q

What are the contents of the Mallory Denk bodies made of

A

Keratins 8 and 18 in complex with proteins such as ubiquitin

150
Q

What are the morphological characteristics of the neutrophil reaction seen in alcoholic hepatitis

A

Neutrophils penetrate the lobule and accumulate around the Mallory Denk bodies

151
Q

What are the histological findings of alcoholic steatofibrosis

A
  • Fibrosis of the central vein and space of Disse, resulting in a chicken wire pattern
  • Continues use results in perisinusoidal scarring leading to mucronodular or Leanne’s cirrhosis
  • Can have the loss of hepatocytes and fatty accumulation
152
Q

Which gender is more likely to develop hepatic injury and what is the cause

A

Women, because the estrogen dependent response to LPS in the liver

153
Q

Which nationalities are more likely to develop cirrhosis

A

African Americans

154
Q

Polymorphisms in which genes can cause the increased risk for hepatic injury

A

ALDH2

155
Q

What is the response on cells during exposure to alcohol

A

-Steatosis, mitochondrial and cellular membrane dysfunction, hypoxia, and oxidative stress

156
Q

What is the reasoning behind alcohol causing steatosis

A

Shunting of substrates from catabolism toward lipid biosynthesis due to increased NADH

157
Q

What are the biochemical results of alcohol ingestion

A
  • Increased NADH
  • Decreased assembly and secretion of lipoproteins
  • Increased free fatty acids
158
Q

What are the methods in which alcohol can cause cellular dysfunction

A
  • Acetaldehyde causes lipid peroxidation and skeletal membrane dysfunction
  • CYP450 metabolism causes production of ROS
  • impaired methionine production and decreased glutathione
159
Q

Alcoholic hepatitis can usually arise following which event

A

Heavy bout of drinking

160
Q

What are the common serum finding of alcoholic liver disease that can differentiate it from other chronic liver diseases

A

-AST elevated 2:1 over ALT

161
Q

What are the common causes of death in end stage alcoholics

A
  • Hepatic coma
  • massive GI bleed
  • Intercurrent infection
  • Hepatorenal syndrome
  • Hepatocellular carcinoma
162
Q

What is the most common cause of chronic liver disease in the US

A

NAFLD

163
Q

What condition does NAFLD increase the risk for and how is it different from the other forms that cause it

A

Increased risk for hepatocellular carcinoma, but does so without the presence of scarring like the other causes

164
Q

What about the cells in NAFLD place it at a higher risk for dysfunction

A
  • Increased production of proinflammatory cytokines

- Increased risk for lipid peroxidation generated by oxidative stress

165
Q

Which pathway correlates with the amount/stage of fibrosis in NAFLD

A

Shh

166
Q

What are the 4 conditions that at least one must be present to be considered for metabolic syndrome

A
  • DM
  • Impaired glucose tolerance
  • Impaired fasting glucose
  • insulin resistance
167
Q

What are the conditions that 2 must be present to be considered for metabolic syndrome

A
  • BP >140/90
  • waist/hip > .9
  • BMI >30
  • dyslipidermia (TG > 1.965, HDL 20 microgram/min)
168
Q

pathological steatosis is defined as having what

A

More than 5% of hepatocytes

169
Q

In NASH, how is it differentiated from NAFLD

A

Mononuclear cells are more prominent, Mallory-Denk bodies are less prominent

170
Q

Previous cryptogenic cirrhosis cases are now being thought to represent which condition

A

Burned out NAFLD

171
Q

How does pediatric NAFLD different from adult cases

A
  • More diffuse steatosis
  • Portal rather than central fibrosis
  • Portal and parenchymal mononuclear inlitration rather than neutrophils
172
Q

What is the most reliable diagnosis for NAFLD and NASH

A

Liver biopsy

173
Q

What serum levels are elevated in 90% of patients with NASH

A

ALT and AST

174
Q

What is the frequent cause of death in patients with NASH

A

Cardiovascular disease

175
Q

What is the name of the stain that is used to show the chicken wire pattern in steatosis

A

Masson trichromatic stain

176
Q

What is the general mechanism of hemochromatosis

A

Excessive iron absorption that gets deposited in the parenchymal organs such as liver pancreas, as well as heart, joints and endocrine organs

177
Q

What occurrence leads to secondary hemochromatosis

A

Excess blood transfusions or other parenteral administration of iron

178
Q

Which three findings are exhibited in fully developed cases of hemochromatosis

A
  • Micronodular cirrhosis in all patients
  • DM in 75 % of patients
  • Abnormal skin pigment in 75% of patients
179
Q

What is the common age that hemochromatosis will emerge in men, and what about women

A

40s and 50s for men

Later for women due to menstration

180
Q

What are the mechanism that excessive iron in hemochromatosis causes damage

A
  • Lipid peroxidation bur iron catalyzed free radicals
  • Stimulation of collagen formation by the activation of stellate cells
  • Integration of reactive oxygen species with DNA, leading to injury and HCC
181
Q

What is the main regulator of iron absorption and the gene responsible for it

A

Hepcidin, which is coded by HAMP game

182
Q

What are the conditions that will increase the coding of hepcidin

A

Inflammatory cytokines and iron

183
Q

What are the conditions that will decrease the amount of coding for hepcidin

A
  • Iron deficiency
  • Hypoxia
  • ineffective erythropoiesis
184
Q

What is the mechanism of action for hepcidin

A

Binds to the efflux channel ferroportin, which causes the internalization and proteolysis and the inhibition of release from intestinal cells and macrophages. Overall, this results in the lower plasma levels of iron

185
Q

What are the proteins that regulate the level of hepcidin

A
  • HJV
  • TFR2
  • HFE
186
Q

Most adult forms of hemochromatosis are caused by which mutation and what is the function of that protein

A

HFE, which codes and HLA class 1 like molecule that controls intestinal absorption of dietary iron by regulating the levels of hepcidin synthesis.

187
Q

What is the mutation in the HFE gene that causes hemochromatosis

A

Cytosine to tyrosine at 282 (aka C282Y)

188
Q

Which hemochromatosis most common mutation gene is most common in which patient group

A

HFE mutation most common in white patients

189
Q

Which mutations causing hemochromatosis is more likely to cause severe juvenile hemochromatosis

A

HAMP and HJV

190
Q

Which condition is characterized by the following conditions:

  • Deposition of hemosiderin in liver, pancreas, myocardium etc
  • Cirrhosis
  • pancreatic fibrosis
A

Hemochromatosis

191
Q

What is the stain used to identify hemochromatosis and what is being identified

A

-Prussian blue stain looking for hepatocellular iron

192
Q

What are secondary conditions seen with hemochromatosis

A
  • Pseudogout

- Testes are small and atropic

193
Q

What are the clinical manifestations of hemochromatosis

A
  • Hepatomegaly
  • abdominal pain
  • abnormal skin color
  • DM due to pancreatic damage
194
Q

What are the two causes of death usually in patients with hemochromatosis

A

HCC and cardiac disease

195
Q

Which condition does hemochromatosis predispose patients for

A

200x more likely to develop HCC

196
Q

What is the effect of fixing the iron overloading in hemochromatosis

A

Risks still remain for the HCC because of the DNA damage already being done

197
Q

What is the presenting features of neonatal hemochromatosis and what is the cause

A

Cause is not hereditary, but normally damage to the liver in utero

  • Severe liver disease
  • Extrahepatic hemosiderin Deposition
198
Q

How is neonatal hemochromatosis detected

A

Buccal biopsy for extra hepatic deposition

199
Q

What are the most common causes of secondary hemochromatosis

A

Ineffective erythropoiesis:

  • thalassemia
  • myelodyspastic syndromes
200
Q

Wilson’s disease is caused by a mutation in which gene

A

ATP7B

201
Q

What is the heritability of Wilson’s disease

A

Autosomal recessive

202
Q

In Wilson disease, what is being deposited and in what common locations

A

-Copper, normally in the eye, brain, liver

203
Q

What is the mechanism of disease in Wilson disease

A

ATP7B gene loss results in the decreased expression of copper transporters that eliminate excess copper

204
Q

What are the three mechanisms that excess copper causes toxicity

A

1-Formation of free radicals by the Fenton reaction
2-Binding to sulfhydryl groups of proteins
3-Displacing other metals in hepatic metalloenzymes

205
Q

Which stains are used for the identification of copper in Wilson disease

A 
Rhodamine stain (copper)
Orcein stain (copper assoacited proteins)
206
Q

Wilson’s disease primarily affects which portion of the brain

A

Basal ganglia, mainly the putamen

207
Q

Which conditions may be confused with Wilson disease

A

Parkinson

208
Q

What are the diagnostic features of Wilson disease

A
  • Decreased serum ceruloplasm
  • Increased hepatic copper content (most sensitive/accurate)
  • increased urinary excretion of copper (most specific)
209
Q

What is the heritability of alpha-1 antitrypsin deficiency

A

Autosomal recessive

210
Q

What the organs affected in alpha-1 antitripsin deficiency

A

Liver (over accumulation of misfolded proteins)

Lungs (lack of Alpha1AT to inhibit elastase)

211
Q

What is the most common clinically significant mutations

A

PiZ coding for the PIZZ protein

212
Q

What is the most commonly diagnosed inherited hepatic disorder in infants and children

A

Alpha1- Antitrypsin deficiency

213
Q

Where in the liver does the misfolded PIZZ protein accumulate

A

ER of the hepatocytes

214
Q

What is the stain used for identifying alpha-1 antitrypsin deficiency

A

PAS stain with diastase

215
Q

Which histological feature is characterized in alpha 1 antitrypsin

A

Cytoplasmic globular inclusions in the hepatocytes, which will stain magenta

216
Q

In patients with alpha1 AT deficiency, which activity should be avoided at all costs

A

Smoking, as it will increase the rate of emphysema

217
Q

What are the properties of unconjugated bilirubin properties with the solubility, toxicity, and ability to be excreted

A

Insoluble in water, so is tightly bound to albumin
No not be excreted in urine
Toxic

218
Q

What are the properties of conjugated bilirubin with regards to solubility, toxicity, and ability to be excreted in urine

A
  • Water soluble, and loosely bound to albumin
  • Non-toxic
  • Can be excreted via urine (when levels are high)
219
Q

What is the function of the protein UGT1A1

A

Hepatic conjugating enzyme

220
Q

What are the heritability of the diseases that results in excess conjugated bilirubin

A

Autosomal recessive

221
Q

What are the only conditions that result in predominantly conjugated hyperbilirubinemia, and was is the result

A

Usually innocuous

  • Dubin Johnson syndome
  • Rotor Syndrome
222
Q

What is cholestasis

A

Impaired bile formation and bile flow that gives rise to accumulation of bile pigment in the hepatic parenchyma

223
Q

What are the clinical presentations of a patient with cholestatis

A
  • Jaundice
  • Pruritus
  • Skin xanthomas
  • intestinal malabsorption of vitamins A,D,K,E
224
Q

What are the clinical lab findings that would indicate cholestasis

A

Elevated alkaline phosphate

Elevated glutamyl transpeptidase (GGT)

225
Q

Which conditions may histologically have fine foamy appearance, looking like “feathery degeneration” as a result of bile pigmentation accumulation

A

Cholestasis

226
Q

What is the most common cause of bile duct obstruction in adults

A

-Extrahepatic cholelithiasis

227
Q

What are the three main causes of bile duct obstruction

A
  • Extrahepatic cholelithiasis
  • Malignancies of biliary tree/head of pancreas
  • strictures from procedures
228
Q

What is ascending cholangitis

A

Secondary bacterial infection of the biliary tree

229
Q

What is the clinical presentation of cholangitis

A

Fever, chills, abdominal pain, and jaundice

230
Q

What is the most severe form of cholangitis

A

Suppurative, where the purulent bile fills and distends the bile ducts

231
Q

What is the histological hallmark of ascending cholangitis

A

Influx of peridcutal neutrophils directly into the bile duct epithelium and lumen

232
Q

What are the histological findings seen in acute biliary obstruction

A
  • neutrophil influx into the bile duct epithelium
  • feathery degeneration (from cholestasis)
  • Mallory-Denk bodies
  • formation of bile infarcts
233
Q

Which condition is most likely to cause cholestasis of sepsis

A

-Response to circulating microbial products, especially those in gram neg bacteria

234
Q

What is the most common form of cholestasis

A

Canalicular cholestasis (around the centrilobular canaliculi)

235
Q

What is the prognosis of ductular cholestasis

A

Poor, especially if there are bile plugs present, causing the dilation of tracts, often accompanying or proceding septic shock

236
Q

What is hepatolithiasis

A

Disorder of intrahepatic gallstones that leads to repeated cases of ascending cholangitis, leading to progressive inflammatory destruction of hepatic parenchyma

237
Q

Which condition is more likely to develop during hepatolithiasis

A

Cholangiocarcinoma

238
Q

What is the only common location for hepatolithiasis

A

Asia, aka oriental cholangitis

239
Q

What is the morphology for hepatolithiasis

A

Pigmented calcium bilirubinate stones in a distended intrahepatic bile duct

240
Q

Which condition produces histological findings that look like irregular shapes, similar to jigsaw puzzle shapes

A

Biliary cirrhosis

241
Q

What are the major causes of prolonged conjugated hyperbilirubinemia in neonates

A
  • biliary atresia

- neonatal Hepatitis

242
Q

Why is it crucial to differentiate between biliary atresia and neonatal hepatitis

A

Because the treatments are different:

  • Biliary atresia (Kasai procedure to fix)
  • Neonatial hepatitis (procedures may cause complications)
243
Q

What are the clinical presentations of neonatal hepatitis

A
  • Jaundice
  • Dark urine
  • acholic stools
  • hepatomegaly
244
Q

What are the histological findings of neonatal hepatitis

A
  • Giant cell transformation of hepatocytes
  • hepatocellular and canalicular cholestasis
  • mononuclear infiltrates of portal areas
  • reactive changes in Kupffer cells
  • extramedullary hepatopoiesis
245
Q

What is biliary atresia

A

Complete or partial obstruction of the lumen of the Extrahepatic biliary tree within the first 3 months of life

246
Q

What is the number one cause of death from liver disease in early childhood and accounts for 50% of children referred for liver transplants

A

Biliary atresia

247
Q

What are the common conditions seen in association with the fetal form of biliary atresia

A

Abnormal development of organs:

  • lack of laterality of Thoracic duct
  • inversus malrotation of abdominal viscera
  • interrupted IVC
  • polyspenia
  • Congentical eart disease
248
Q

What is the overall cause of fetal form of biliary atresia

A

Aberrant intrauterine development of the extrahepatic biliary tree

249
Q

What is the most common cause of biliary atresia

A

Perinatal form

250
Q

What is the pathogensis of the perinatal form of biliary atresia

A

Normal development of the biliary tree, but is destroyed following birth.

251
Q

Which conditions of biliary atresia are correctable

A
  • Limited to the common duct (Type 1)

- Limited to the right and left hepatic bile ducts (Type 2)

252
Q

Which condition of biliary atresia is not correctable

A

Type 3, obstruction of the ducts at or above the porta hepatic

253
Q

What are the clinical presentations of biliary atresia

A
  • Normal north weight and postnatal weight
  • Normal stools will begin to change to acholic stool
  • Death within 2 years without transplant
254
Q

What is the primary biliary cirrhosis characterized by

A

No suppurative, inflammatory destruction of small and medium sized hepatic bile ducts. Large ducts are not involved

255
Q

Where is primary biliary cirrhosis most prevalent geographically

A

Northern European and Minnesota

256
Q

How related is primary biliary cirrhosis in families

A

Increased risk

257
Q

What is the most characteristic laboratory finding in primary biliary cirrhosis

A

Antimitochondrial antibodies

258
Q

What are the target of the most commonly seen antibodies in primary biliary cirrhosis

A

E2 of the pyruvate dehydrogenase complex

259
Q

What is the histological finding in the condition of primary biliary cirrhosis

A
  • Florid duct lesions, where the interlobular bile ducts are actively being destroyed by lymphocytes
  • Periportal/periseptal cholestasis
260
Q

What is a distinguished organ size characteristic of primary biliary cirrhosis

A

Hepatomegaly

261
Q

What is a treatment for primary biliary cirrhosis that slows down the progression of the disease

A

Ursodeoxychilic acid

262
Q

What are the symptoms seen as primary biliary cirrhosis progresses

A
  • Skin hyper pigmentation
  • xanthelasmas
  • steatorrhea
  • Vitamin D osteomalacia
263
Q

What is primary sclerosing cholangitis characterized by

A

Inflammation and obliterative fibrosis of the intrahepatic and extrahepatic bile ducts

264
Q

Which conditions are commonly associated with primary sclerosing cholangitis

A

IBD, and UC

265
Q

Which HLA is associated with primary sclerosing cholangitis

A

HLA-B8

266
Q

Which conditions is commonly seen when there are degenerating bile ducts entrapped in an “onion skin” scar

A

primary sclerosing cholangitis

Aka a tombstone scar

267
Q

What is the laboratory finding that may accidentally find primary sclerosing cholangitis

A

Elevated levels of alkaline phosphate

268
Q

What are choledochal cysts

A

Congenital dilations of the common bile duct

269
Q

Which patient group is commonly seen to have choledochal cysts

A

Female Children before age of 10

270
Q

The development of Choleductal cysts increase the risk of which condition in older patients

A

Bile duct carcinoma

271
Q

What are the common conditions seen with fibropolycystic disease

A

1-Von meyeberg complexes (bile duct hamartomas)
2- Small biliary cysts (Caroli disease)
3- Congentical hepatic fibrosis

272
Q

What are the conditions assoacited with fibropolycystic disease caused by

A

Ductal plate malformations

273
Q

Fibropolycystic liver disease commonly occurs with which condition

A

Autosomal recessive polycystic renal Disease

274
Q

Which gene is involved in polycystic kidney disease as well as fibrocystic liver disease

A

Polycystin

275
Q

Patients with fibrocystic liver disease are at a higher risk for which condition

A

-Cholangiocarcinoma

276
Q

When will a hepatic artery thrombosis cause infarction

A

In transplanted patients because there is only arterial supply to the biliary ducts

277
Q

In those patients with extrahepatic portal vein obstruction, which condition is assoacited 25% of the time, and which underlying condition is commonly present

A

Cirrhosis is present in 25% of cases, with an underlying thrombophlebitis genotype

278
Q

What can the intrahepatic portal vein radicle be abstracted by

A

Acute thrombosis

279
Q

What is the result of intrahepatic portal vein radicles being blocked by an acute thrombosis

A
  • Does not cause an ischemic infarction
  • Causes a sharply demarcated area of red/blue discoloration called the infarct of Zahn
  • Results in severe hepatocellular atrophy and stasis around the sinusoids
280
Q

WHich condition is going to result in the infart of Zahn

A

Acute Thrombotic event in the intrahepatic portal vein radicles

281
Q

What are the results of a small portal vein branch disease

A

Noncirrhotic portal hypertension with portal fibrosis and obliteration of the small portal vein branches

282
Q

What is the most common small portal vein branch obstruction

A

Schistosomiasis, where the eggs lodge and obstruct

283
Q

Small portal vein branch disease seen in East Asia is commonly in which patient group and with which associated condition

A

Female, Japanese, and rheumatologist diseases

284
Q

Which treatments or conditions increase the risk of small portal vein branch disease

A
  • Untreated HIV

- anti-retroviral treatment

285
Q

What is the most common intrahepatic cause of blood flow obstruction

A

Cirrhosis

286
Q

Which conditions can cause sinusoidal occlusion through the liver

A
  • Sickle cell
  • DIC
  • Eclampsia
  • metastatic cancer
287
Q

What is the condition of peliosis hepatis

A

Sinusoidal dilation that causes the efflux of hepatic blood to be impeded

288
Q

What are some causes of peliosis hepatis

A
  • Bartonella

- Sex hormone administration

289
Q

What are fetal outcomes of peliosis hepatis if the underlying cause is not treated

A

-Intraabdominal hemorrhage or hepatic failure

290
Q

Which condition is defined as obstruction of two or more major hepatic veins producing liver enlargement, pain, and ascites

A

Budd Chiari syndrome

291
Q

During Budd-chiari Syndrome, what is the actual mechanism causing damage

A

Increased intrahepatic blood pressure

292
Q

Which conditions are hepatic vein thrombosis associated with

A

myeloproliferative disorders:

  • polycythemia Vera
  • coagulation disorders
  • antiphospholipid antibody syndrome
  • paroxysmal nocturnal hemoglobinuria
  • HCC
293
Q

What is the morphology seen during budd-Chiari syndrome

A

Liver is swollen with a red-purple, tense capsule

-Alternating pattern of hemorrhagic places with those that are regenerating

294
Q

What is the mortality rate in untreated acute hepatic vein thrombosis

A

High

295
Q

What are the primary settings that sinusoidal obstructive syndrome develops

A
  • Following allogenic hematopoietic stem cell transplantation within the first 3 weeks
  • cancer patients receiving chemotherapy
296
Q

What is the pathogenesis of sinusoidal obstructive syndrome

A

Toxic injury to the sinusoidal endothelium, which obstructs the blood flow

297
Q

What is the histological characteristic of sinusoidal obstruction syndrome

A

Obliteration of the terminal hepatic venules by subendothelial swelling and collagen deposition

298
Q

What is the cause of passive congestion of the liver

A

Right sided heart failure

299
Q

What is the morphology of the liver following right sided heart failure

A

Congestion of the centrilobular sinusoids

300
Q

What is the cause of the appearance of the nutmeg liver

A

Right sided heart failure provides the passive congestion (red portion) while the left sided heart failure results in hypoxia (orange color)

301
Q

How many days after transplantation does graft versus host disease occur with liver transplantation

A

10 to 50 days following

302
Q

What are the morphological changes seen in graft versus hosts disease in the liver

A

Hepatitis with necrosis of hepatocytes and bile duct epithelial cell, inflammatory cells in the bile duct epithelium

303
Q

What is the final pathogenesis of chronic rejection of a liver

A

Obliterative arteriopathy of the small and large arteries, which lead to the ischemic changes in the liver parenchyma, ultimately resulting in vanishing bile duct syndrome

304
Q

What is the most common cause of jaundice in pregnancy

A

Viral hepatitis

305
Q

How does pregnancy change the course of a viral hepatitis infection, and what is the exception

A

Does not change the course of the viral hepatitis infection, except for HEV, which causes more severe of a cause in pregnant women, leading to 20% fatality

306
Q

What are the presentations of preeclampsia

A
  • Maternal hypertension
  • Proteinuria
  • Peripheral edema
  • Coagulataive abnormalities
307
Q

What are the clinical presentations of eclampsia

A

Hyperreflexia and convulsions

308
Q

What are the histological findings of preeclampsia

A

Periportal sinusoids containing fibrin deposits associated with hemorrhage into the space of Disse, which leads to Periportal coagulative necrosis

309
Q

When do pregnant women usually present with acute fatty liver of pregnancy

A

latter half, usually the third trimester

310
Q

What histological and morphological finding can occur and usually resulting in fatality

A

Subscapular hematoma under the Glisson capsule, which can rupture

311
Q

What is the proposed cause of acute fatty liver of pregnancy

A

Mother lacks long chain 3-hydroxyacyl CoA dehydrogenase, so when it is produced by the fetus, it causes damage to the mother

312
Q

What is the onset of intrahepatic cholestatis of pregnancy

A

Third trimester

313
Q

What are the clinical presentations of intrahepatic cholestasis of pregnancy

A

Darkening of the urine
Occasional light stools
Jaundice
Large increase in the level of bile salts

314
Q

What is focal nodal hyperplasia and it’s characteristic

A
  • Well demarcated, but poorly encapsulated nodule
  • In young to middle age adults
  • Central stellate scaring
315
Q

Nodular regenerative hyperplasia is most commonly associated with which conditions

A

HIV infected people

Rheumatic diseases such as SLE

316
Q

What is the most common type of benign liver tumors

A

Cavernous hemangioma

317
Q

What are the types of benign liver neoplasm

A
  • Cavernous hemangiomas

- Hepatocellular adenomas

318
Q

What is the medical emergency associated with hepatocellular adenomas

A

Intraabdominal bleeding

319
Q

What would place a patient at a higher risk for hepatocellular adenomas

A

Oral contraceptives

Anabolic steroids

320
Q

What is the increased risk factor of the oral contraceptives for hepatocellular adenoma

A

30-40x

321
Q

The majority of hepatocellular adenomas have a mutation of what

A

Inactivating somatic mutation of HNF1-alpha

322
Q

How many mutations are required for the patients with hepatocellular adenoma tumors with the MODY3

A

A second somatic mutation

323
Q

Which form of the hepatocellular adenomas are at the highest risk of becoming malignant

A

Beta-catenin activated hepatocellular adenomas

324
Q

Which condition are inflammatory hepatocellular adenomas associated with

A

NAFLD

325
Q

What is the only hepatocellular adenoma that does not have a risk of becoming malignant

A

HNF1 alpha

326
Q

The inflammatory hepatocellular adenoma is associated with which factors

A

Gp130, IL6

Via JAKSTAT signaling

327
Q

Which tumor is present if there is complete absence of Liver Fatty acid binding protein (LFABP)

A

HNF1-alpha hepatocellular adenoma, and immunostaining for it is diagnostic

328
Q

Which tumor is present if with immunostaining, there is a high presence of glutamine synthetase

A

Beta catenin hepatocellular adenoma (targets downstream GLU synthetase)

329
Q

Which factors are overexpressed in the inflammatory hepatocellular adenomas

A

-CRP and serum amyloid A

330
Q

What is the most common tumor of early childhood

A

Hepatoblastoma

331
Q

What are the cell types present in the epithelial type of hepatoblastoma

A

-small polygonal fetal cells that form acini, tubules

332
Q

What are the cells included in the mixed epithelial and mesenchymal type of hepatoblastoma

A

-osteosarcoma, cartilage, or striated muscle

333
Q

What is the characteristic pathway activated in hepatoblastoma

A

WNT

334
Q

Which genes are commmonly mutated in hepatoblastoma

A
  • APC
  • Beta catenin
  • FOXG1
335
Q

Which familial conditions normally can develop hepatocellular adenomas

A
  • Familial adenomastous polyposis

- Beckwith-Wildemann syndrome

336
Q

Most hepatocellular carcinomas are associated with areas with this endemic infection

A

HBV

337
Q

In cases with patients who have HCV, what comes before the malignancy HCC

A

Cirrhosis

338
Q

What gender is more likely to develop hepatocellular carcinoma

A

Male

339
Q

What are the most common setting for the emergence of HCC

A

Chronic liver diseases

340
Q

In Asian and African countries, what can HBV synergize with to increase the risk of HCC

A

Aflatoxin

341
Q

Which metabolic diseases increase the risk of hepatocellular carcinoma

A
  • Metabolic syndrome, with the obesity, DM, NAFLD
  • Hemochromatosis
  • alpha1-AT
342
Q

What are the two most common early mutations in the development of hepatocellular carcinoma

A

P53 and Beta catenin

343
Q

Which mutation in HCC are more likely to be associated with non HBV and more genetic instability

A

Beta catenin

344
Q

What mutation in HCC is strongly assocaited with aflatoxin

A

P53

345
Q

What cell size change is directly a premalignant sign

A

Small cell change

346
Q

What cell size change associated with hepatitis B is a premalignant

A

Large cell size change

347
Q

What are the histological findings of large cell changes

A

Normal nuclear to cytoplasmic ratio but scattered normal hepatocytes with larger than normal nuclei

348
Q

What are the histological changes seen in small cell changes

A

High nuclear to cytoplasmic ratio and the cells are separated by a thickened plates

349
Q

In high grade dysplasia can nodules, what is the characteristic of the blood supply and how does this compare to the low grade

A

High grade- arteries dominate

Low grade- arteries and veins

350
Q

What is the most likely route of extrahepatic masses to spread

A

Arterial supply

351
Q

Where do primary liver tumors preferentially spread

A

Lungs, usually very late in the course

352
Q

What are the clinical presentation of hepatocellular carcinomas

A

Fatigue, weight loss, hepatomegaly, abdominal pain in the URQ

353
Q

Elevations of which serum component is elevated in advanced hepatocellular carcinomas

A

Serum alpha-fetoprotein

354
Q

What are the histological findings of fibrolamellar carcinoma

A

Large, hard “scirrhous” tumor with fibrous bands

-Cords and nests of oncocytic hepatocytes separated by dense bundles of collagen

355
Q

What are the 4 causes of death in those patients with hepatocellular carcinoma

A

1-cachexia
2-GI or esophageal varices bleeding
3-liver failure and coma
4-rupture of the tumor

356
Q

What is the cholangiocarcinoma

A

Primary malignant tumor of the biliary tree/ducts

357
Q

What areas and which parasite are associated with higher levels of cholagiocarcinoma

A

in the southeast Asian countries where the liver flukes are endemic

358
Q

Which conditions have an increased risk of developing cholangiocarcinoma

A
  • NAFLD
  • HBV and HCV
  • liver flukes (opisthorchis and Clonorchis)
  • Chronic inflammation ofthe bile ducts
359
Q

The majority of choleangiocarcinomas are what type and in which location

A

50 to 60% are Klatskin tumors, which are at the junction of the right and left hepatic ducts (aka perihilar)

360
Q

What is the prognosis of choleangiocarcinomas

A

very very bad

361
Q

What is the most common premalignant lesion for cholangiocarcinoma

A

Biliary intraepithelial neoplasia 3 (BilIN-3)

362
Q

What type of tumor is choleangiocarcinomas and which product is secreted

A

Adenomas, which secrete mucin

363
Q

What are the typical histological findings of a choleangiocarcinoma

A
  • Desmoplasia

- lymphovascular and perineural invasion

364
Q

Which liver malignancy will form a wreath like patter around a central trapped nerve

A

Perineural

365
Q

What are the causes of a liver angiosarcoma forming

A
  • Vinyl chloride
  • Arsenic
  • Thorotrast
366
Q

What are hepatic lymphomas associated with and which form do most take

A
  • HCV, HBV, HIV, PBC

- Diffuse B cell lymphomas

367
Q

What are the common locations that metastasizing to the liver is common

A

-Colon, Breast, lung, pancreas

Robbins Pathology GI (Chptr 16,17,18,19) (32 decks)

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