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GI II - EXAM 2 > Liver Pathology I - SRS > Flashcards

Liver Pathology I - SRS Flashcards

1
Q

What enters the liver at the porta hepatis?

A
  1. Portal vein
  2. hepatic artery
  3. bile duct
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2
Q

Identify the structures shown.

A
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3
Q

What is the normal diameter of an anatomic liver lobule?

A

1-2 mm

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4
Q

Identify the indicated structures

A
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5
Q

What is the space of Disse?

Obstruction here can lead to what?

A

Space between Sinusoids and the hepatocytes.

Contains lymph and interstitial fluid.

Can lead to portal HTN

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6
Q

Identify the blanked out structures

A

Top: hepatocyte

Bottom: Bile canaliculi

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7
Q

Identify

A

Left: Lumen of the sinusoid

Right: space of disse

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8
Q

The endothelial layer is fenestrated and not supported by a basal lamina. What are the hepatocytes directly exposed to?

A

Plasma

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9
Q

Where are we here?

A

Lumen of a hepatic sinusoid with the endothelial cell coating, displaying the typical fenestrations arranged as clusters and forming the so-called sieve plates.

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10
Q

What cells are found in the cords and sinusoids?

A

Hepatocytes

sinusoidal endothelial cells

kupffer cells

stellate (ito) cells

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11
Q

What is the role of the stellate cell?

A

Storage of fat, vitamin (A in particular), fibrous tissue metabolism

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12
Q

What makes up the portal triad?

A

Portal vein

hepatic artery

bile duct (and lymphatics)

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13
Q

Identify

A

Top: Portal triad

Bottom: Central Vein

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14
Q

In the liver acinus, where is the highest oxygen tension?

A

Zone I

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15
Q

Identify the indicated structures.

A

Green = Zone I

Orange = Zone II

Red = Zone III

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16
Q

From the portal triad, describe the flow of blood.

A

Hits zone one first, highest O2 concentration here.

Goes then to zone II and then Zone III, before finally reaching the central vein to drain.

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17
Q

What zone has the lowest O2 concentration?

A

Zone III

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18
Q

What is the “supporting structure” for the hepatocytes?

A

Reticulin

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19
Q

List as many of the metabolic functions of the liver as you can.

A
  • Formation and excretion of bile during bilirubin metabolism
  • Regulation of carbohydrate homeostasis
  • Lipid synthesis and secretion of plasma lipoproteins
  • Control of cholesterol metabolism
  • Formation of urea, serum albumin, clotting factors, enzymes, and numerous other proteins
  • Metabolism or detoxification of drugs and other foreign substances
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20
Q

What are the major causes of liver injury?

A
  • Infection
  • Immune mediated
  • Drug and Toxin
  • Metabolic
  • Genetic
  • Autoimmune cholangiopathy
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21
Q

What are two big drug/toxin causes of liver injury?

A

Acetaminophen

Ethanol

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22
Q

What are three examples of genetic causes of liver injury?

A

–Hemochromatosis

–Wilson’s disease

–Alpha-1 antitrypsin deficiency

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23
Q

What are two examples of autimmune cholangiopathy?

A

–Primary biliary cirrhosis

–Primary sclerosing cholangitis

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24
Q

What is the definition of acute liver failure?

A

Evidence of coagulation abnormality and any degree of mental alteration in a patient without pre-existing cirrhosis and with an illness less than 26 weeks duration.

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25
Q

Acute Hepatic Failure is onset of liver failure within 26 weeks after onset of new liver disease defined by evidence of impaired liver function with increased PT and encephalopathy.

What amount of hepatocytes must be lost to manifest this way?

What is the mortality rate?

What is the treatment approach?

A

Caused by: >80% loss of hepatocytes

Mortality rate: 40-80%

Approach: Hospitalize and consider liver transplantation

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26
Q

What does fulminant hepatic failure describe?

A

used to describe the development of encephalopathy within 8 weeks of the onset of symptoms

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27
Q

What are five manifestations of acute liver failure?

A
  1. •Jaundice
  2. •Neurologic symptoms
  3. •Encephalopathy
  4. •Portal hypertension
  5. •Hepatorenal syndrome
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28
Q

What can the presentation of hepatic encephalopathy look like?

A

•can range from sleep disturbance –> lethargy –> deep somnolence –> coma

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29
Q

What type of neurologic symptoms can acute liver failure cause?

A

•symptoms can include a asterixis (flapping tremor) and hyperactive reflexes.

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30
Q

What is hepatorenal syndrome triggered by?

A
  • thought to be triggered by vasodilation in the splanchnic circulation leading to decreased renal perfusion and glomerular filtration.
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31
Q

How do we determine the extent of hepatocyte injury in the lab?

A

AST, ALT

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32
Q

What laboratory tests do we use to identify cholestatic biliary tract dysfunction?

A

–Serum bilirubin (direct and indirect)

–Alkaline phosphatase

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33
Q

What do we use to assess the sythentic capabilities of the liver?

What are the half lives of these things?

A

–Serum albumin (20 day half life)

–Coagulation factors (5-48 hrs half life)

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34
Q

Liver failure may follow acute injury or chronic injury, but may also occur as an acute insult superimposed on an otherwise well-compensated chronic liver disease.

What is the mnemonic for causes of acute liver failure?

A

–A: Acetaminophen, hepatitis A, autoimmune hepatitis

–B: Hepatitis B

–C: Hepatitis C, cryptogenic

–D: Drugs/toxins, hepatitis D

–E: Hepatitis E, esoteric causes (Wilson disease, Budd-Chiari)

–F: Fatty change of the microvesicular type (fatty liver of pregnancy, valproate, tetracycline, Reye syndrome)

He said he wasn’t sure if this would be worth a shit though, so hey, whatever.

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35
Q

Liver failure entails what serious and potentially fatal sequelae?

A

Coagulopathy

encephalopathy

Portal HTN

Esophageal Varices

Hepatorenal syndrome

Portopulmonary HTN

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36
Q

What determines the presence of chronic hepatitis?

A

Persistent liver disease (AKA)

lasting for more than 26 weeks

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37
Q

Hepatitis may evolve through fibrosis to what outcomes?

A
  1. •Cirrhosis
  2. •Complications of cirrhosis
  3. •Hepatocellular carcinoma
38
Q

Acute hepatitis may be clinically asymptomatic with only abnormal LFTs. If symptomatic what can been seen for the following?

  1. Constitutional symptoms
  2. Physical Findings
  3. Rare findings
A
  1. Nonspecific constitutional symptoms
  • –Fever
  • –Nausea/vomiting
  • –Fatigue
  1. Physical findings
  • –Jaundice
  • –Tender liver
  • –Altered mental status/coma (hepatic encephalopathy)
  • –Bleeding
  1. Uncommon
  • –Headaches, myalgias, arthritis
  • –Rash, urticaria, arthritis
39
Q

Symptoms of acute hepatitis can be proportional to what?

A

Degree of ALT/AST elevation

40
Q

Describe the AST/ALT levels in chronic liver disease

A

•Liver injury tests (AST/ALT) tend to be low to moderate but persist for months/years

41
Q

Daily symptoms in chronic liver disease may be mild or even absent. Does regeneration occur?

What happens in the long run?

A
  • Hepatic regeneration occurs but may or may not equal injury
  • Long-term: new symptoms may arise due to liver dysfunction and/or as consequences of cirrhosis
42
Q

What are 7 histological manifestations of liver injury?

A
  1. •Inflammation
  2. •Hepatocellular injury (reversible)
  3. •Necrosis and apotosis (cell death)
  4. •Regeneration
  5. •Fibrosis
  6. •Neoplasia
43
Q

Identify

A

Top: Portal tract

Left: Sinusoids

Right: Central Vein

44
Q

In chronic liver failure, what inflammatory cells will you see?

A

Lymphocytes - lots in the portal tract

45
Q

Where are the inflammatory cells in acute hepatitis?

A

Lobular areas

46
Q

What do you see here?

What are four common causes of this?

A

Hepatocellular injury with steatosis.

  1. non-alcoholic fatty liver
  2. alcoholism
  3. drugs
  4. viruses
47
Q

What is microvesicular steatosis associated with?

A

Reye syndrome

Tetracycline toxicity

fatty change of pregnancy

48
Q

What is a relatively new group of patients that has a high level of steatosis?

A

DM II

Obese

Metabolic syndrome

49
Q

What is shown here?

What are three causes?

A

Microvesicular steatosis

  1. Reye syndrome
  2. tetracycline toxicity
  3. fatty change of pregnancy
50
Q

This slide shows hepatocellular injury. What is indicated by the arrows?

What is this often associated with?

A

Top two arrows = Ballooning degeneration

Bottom arrow = clumped intermediate filaments-mallory hyaline

ETOH abuse

51
Q

What is shown here?

What do the arrows show?

A

Acute hepatitis

Top arrow = apoptosis

Bottom arrow = Lobular disarray with mononuclear cell infiltrates

52
Q

What is shown here?

What do the arrows indicate?

What does the arrow head indicate?

A

hepatocellular biliary injury - cholestasis

Arrows = Intracytoplasmic cholestasis

Arrow head = bile in dilated bile canaliculus

53
Q

How long does it take for macros to clear apoptotic bodies in the liver?

A

6-8 hours

54
Q

What is shown here?

A

Hepatocellular biliary injury - cholestasis

Arrow indicates a distended bile canaliculus filled with bilirubin.

55
Q

What do the two sets of arrows indicate?

A

Top = hepatocyte necrosis with eosinophilic remnants of cords and the occasional pyknotic hepatocyte nuclei.

Bottom = viable hepatocytes

56
Q

What are some causes of acute cellular necrosis in the liver?

A

Drugs

certain mushrooms

Viral infection

Autoimmune

57
Q

What is this?

What is it indicative of?

A

Portal inflammation

Chronic viral hepatitis

58
Q

What is shown here?

What is it common in?

What is this previously known as?

A
  • Portal Inflammation with Interface Hepatocyte Injury (Chronic Injury Pattern)
  • Interface hepatitis seen in chronic viral hepatitis
  • previously known as “piecemeal necrosis”
59
Q

What is shown here?

A

Cirrhosis - trichrome stain of the liver demonstrates “bridging fibrosis” and completely surrounded nodules

60
Q

What is “bridging fibrosis”?

A

Fibrosis connecting two or more portal zones

61
Q

Hepatic stellate cells are normally quiescent fat/vitamin A storing cells. In several forms of acute and chronic injury, stellate cells can become activated and transform to what?

A

Highly fibrogenic myofibroblasts

62
Q

If acute or chronic hepatitis persists, scar deposition begins, often in what place?

A

Space of Disse

63
Q

What is the major parenchymal source of excess collagen under abnormal conditions?

A

stellate cells

64
Q

What is shown here?

A

Cirrhosis with parenchymal extinction

65
Q

What is parenchymal extinction d/t?

A

Microscopic areas of ischemia after vascular inflammatory injury and occlusion.

66
Q

In addition to the parenchymal extinction what other changes are seen in cirrhosis?

A

Scarring in areas of hepatocyte dropout and collapse of the lobular unit (PV and CV come close together)

Hepatocyte hyperplasia of viable cells elongate the scars into fibrous septae and bridging fibrosis.

67
Q

What is shown here?

What do the arrows indicate?

What is contained in the structure indicated by the arrows?

A
  1. Cirrhosis
  2. Fibrous septa
  3. Contains preexisting portal tracts, hepatic veins and condensed stroma
68
Q

What characterizes cirrhosis?

A

Diffuse nodular regeneration surrounded by dense fibrotic septae with subsequent parenchymal extinction and collapse of liver structures.

69
Q

Cirrhosis is characterized by diffuse nodular regeneration surrounded by dense fibrotic septae with subsequent parenchymal extinction and collapse of liver structures causing pronounced distortion of hepatic vascular architecture which leads to?

A

Increased resistance to portal blood flow and subsequent portal hypertension.

70
Q

How is cirrhosis classified?

A

Compensated

Decompensated

71
Q

What is the most common cause of death in compensated cirrhosis?

A

Cardiovascular disease

(followed by stroke, malignancy, and renal disease)

72
Q

What are the usual causes of death in patients with decompensated cirrhosis?

A
  1. Portal HTN complications
  2. Hepatocellular carcinoma
  3. sepsis
73
Q

What is a strong prognostic indicator in predicting complications and mortality in patients with both compensated and decompensated cirrhosis?

A

Hepatic Venous Wedge pressure

74
Q

What is the Child-Turcotte-Pugh classification scheme used for?

A

Assessment of prognosis of cirrhosis

75
Q

What are the three CTP classes and their associated scores?

A

A: 5-6 points

B: 7-9 points

C: 10-15 points

76
Q

What are some prehepatic causes of portal HTN?

A

Portal vein thrombosis

narrowing of the portal vein

77
Q

What are some intrahepatic causes of portal HTN?

What is the most common cause?

A

Cirrhosis - accounts for most cases of portal HTN

Sinusoidal obstruction

78
Q

What are some posthepatic causes of portal hypertension?

A

–Severe right-sided heart failure

–Constrictive pericarditis

–Hepatic vein outflow obstruction

79
Q

What are the three mechanisms by which cirrhosis leads to portal HTN?

A
  • Increased resistance to portal flow at the level of the sinusoid
  • Compression of the central vein by perivenular fibrosis and parenchymal nodules
  • Anastomoses between arterial and portal systems imposing high pressure on a low pressure system
80
Q

What are some clinical consequences of portal HTN?

A
  1. Portosystemic venous shunts
  2. Congestive splenomegaly
  3. Ascites
  4. Hepatic encephalopathy
81
Q

What are four important portacaval anastamoses?

A
  1. Para-umbilical
  2. esophageal
  3. retroperitoneal
  4. Rectal
82
Q

What type of cirrhosis is seen with chronic alcoholism?

A

Micronodular

83
Q

What type of cirrhosis is commonly seen with hepatitis B or C infection?

A

Macronodular

84
Q

The development of ascites involves the following components. Describe how each contribute.

  1. Sinusoidal hypertension
  2. Splanchnic vasodilation and hyperdynamic circulation
  3. Decreased plasma oncotic pressure
  4. Increased aldosterone
A
  1. Sinusoidal hypertension drives fluid into the space of Disse where lymph flow exceeds thoracic duct capacity
  2. Splanchnic vasodilation and hyperdynamic circulation leads to increased perfusion pressure of interstitial capillaries causing fluid extravasation in peritoneum
  3. Decreased plasma oncotic pressure - H2O migrates into interstitium
  4. Increased aldosterone leads to increased sodium reabsorption and increased intravascular volume
85
Q

What have we here?

A

Ascites with umbilical hernia from increased abdominal pressure.

86
Q

What are the two chronic liver failure syndromes we covered?

A

Hepatopulmonary Syndrome

Portopulmonary HTN

87
Q

~30% of patients with cirrhosis get hepatopulmonary syndrome. While the pathogenesis is not known, describe the general mechanism by which this occurs.

A
  1. Intrapulmonary vascular dilation
  2. rapid blood flow through pulmonary vasculature
  3. poor Hb oxygenation d/t rapid transit
  4. hypoxia
88
Q

Potopulmonary hypertension is related to portal HTN and may involve excessive pulmonary vasoconstriction. What are two common complaints a patient with this would likely have?

A

–Dyspnea on exertion (DOE)

–Clubbing of fingers

89
Q

Chronic hypoxia causes clubbing, what tissues change in the digits?

Is it reversible?

A

Soft tissue changes have been held responsible for the digital enlargement.

It is reversible.

90
Q
A

GI II - EXAM 2 (11 decks)

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