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Systemic Pathology > Hepatobilliary Pathology > Flashcards

Hepatobilliary Pathology Flashcards

1
Q

Stages of Liver Disease

A

Healthy liver –> fatty liver –> liver fibrosis –> cirrhosis

  • Fatty liver —deposits of fat lead to liver enlargement
  • Liver fibrosis —scar tissue forms
  • Cirrhosis —growth of connective tissue destroys liver cells

Some stages are reversible and some are not

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2
Q

Liver dysfunction

A

Several etiologies

  • Acquired infections and conditions
  • Lifestyle habits
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3
Q

Liver Functions

A

> Produces most of the substances that regulate blood clotting
Produces bile, a compound needed to digest fat and to absorb vitamins A, D, E, K
Removes potentially toxic byproducts of certain medications
Prevents shortages of nutrients by storing vitamins, minerals, and sugar
Metabolizes/breaks down nutrients from food to produce energy when needed
Produces most proteins needed by the body
Helps your body fight infection by removing bacteria from the blood

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4
Q

Symptoms of Liver Dysfunction

A

Yellowing of the skin and eyes (jaundice)

Spider-like blood vessels

Itching

Fluid build-up, swelling of the legs (edema)

Mental confusion

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5
Q

Problems associated with liver disease

A

Risk of bleeding

Alterations in the metabolism/toxicity

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6
Q

Hepatitis definition

A

Inflammation of the liver that may result from Viral hepatitis, infectious mononucleosis, secondary syphilis and tuberculosis, or prolonged use of toxic substances (drugs — acetaminophen, alcohol, ketoconazole (antifungal),
methyldopa, methotrexate)

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7
Q

Viral Hepatitis

A

Acute viral hepatitis is the most common
Different types (A, B, C, D, E, and G)
Diagnostic markers
- White blood cell count, prothrombin time, and liver enzymes
- Lymphocytosis***
o Neutrophils fight bacterial infections, but lymphocytes fight viruses, so
lymphocytes will be elevated

  • Elevation in AST and ALT, alkaline phosphatase
  • Elevated serum bilirubin
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8
Q

Hepatitis A

A

A viral infection of the liver spread when fecal matter enters the mouth
- May last several weeks and can be debilitating, but most people recover completely
- Preventable with careful hand washing, keeping toilets and bathrooms clean, avoiding
infected water sources

Diagnosis: Diagnose with IgM anti hepatitis A virus serology
- Coagulation profile — PT mild elevation is common with HAV infection
- Transmission usually precedes symptoms by 2 weeks when stool concentrations are
highest

Signs and Symptoms

  • Clinical jaundice in 70% of cases with HAV
  • GI — nausea, vomiting, right upper quadrant pain
  • Hepatomegaly and Splenomegaly
  • Clay-colored stools (light colored stools)

Accumulation of bilirubin in the plasma, epithelium, and urine (leading to color change)

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9
Q

Hepatitis B

A

Diagnosis — CBC, coagulation profile, serology, HBV DNA
- Transmission —nonsterile tattooing needles, contaminated dialysis equipment,
contaminated vaccination equipment, nonsterile dental practices, contaminated drug
needs, nonsterile body piercing equipment
- Usually full recovery
- But some people can have different stages
o Non-progressive —chronic
o Progressive — cirrhosis
o Fulminant

o Carrier — asymptomatic

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10
Q

HBeAg

A

—envelop antigen, indicative of active replication

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11
Q

HBsAg

A

—Hepatitis B surface Antigen
o Appears before symptoms
o Disappears in 3- 6 months
o Persists in carriers

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12
Q

Anti-HBs

A

Anti-HBs is the Hep B surface antibody

o Seen after acute disease
o 3-6 months after HBs Ag disappears
o LIFELONG PROTECTION —Immunity
o Vaccination

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13
Q

Anti-HBc — Anti HBc Antibody

A

Total hepatitis B core antibody
o Appears at the onset of symptoms in acute Hep B and persists for life
o Indicates previous or ongoing infection with hepatitis B virus in an undefined
frame

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14
Q

IgM anti HBc

A

Positivity indicates recent infection with hepatitis B virus less than 6 months
o Acute infection

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15
Q

What is the susceptibility for Hep. B in a patient with:
HBsAg (-)
Anti-HBc (-)
Anti-HBs (-)

A

SUSCEPTIBLE

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16
Q

What is the susceptibility for Hep. B in a patient with:
HBsAg (-)
Anti-HBc (+)
Anti-HBs (+)

A

Immune due to hepatitis B

vaccination

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17
Q 
What is the susceptibility for Hep. B in a patient with:
HBsAg (+)
Anti-HBc (+)
IgM anti-HBc (+)
Anti-HBs (-)
A

Acutely infected

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18
Q 
What is the susceptibility for Hep. B in a patient with:
HBsAg (+)
Anti-HBc (+)
IgM anti-HBc (-)
Anti-HBs (-)
A

Chronically infected

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19
Q

Hepatitis C Virus

A

ssRNA virus

Diagnosis — antibodies, serum markers, and viral genotyping
- Antibodies are not protective
o Can get the disease again!
- 55-85% develop chronic disease
- More than 75% of American adults with Hep C are baby boomers
o A big proportion, and a worldwide problem!

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20
Q

Extra-hepatic manifestations of HCV

A
  • Vasculitis
  • Renal complications
  • Skin manifestations

ex.
-Spider angiomata
- Caput medusa
- Terry nails —white nails with a “ground glass” appearance and small bands of normal
pink nail along the top edges

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21
Q

Extra-hepatic manifestations of HBV

A
  • PAN — polyarteritis nodosa
  • Systemic necrotizing vasculitis of medium or occasionally small muscular arteries
  • Multiple aneurysms
  • Transmural necrotizing inflammation — fibrinoid necrosis
  • Affects middle aged or older adults
  • Pathogenesis — idiopathic
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22
Q

Presentation of HBV

A
  • Weight loss
  • Myalgia, weakness, leg tenderness
  • Polyneuropathy or mononeuropathy
  • Elevated diastolic BP >90mmHg
  • Positive HBV infection
  • Arteriographic abnormality
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23
Q

PAN (polyarteritis nodosa)

A

Mononeuritis with motor and sensory deficits

  • Asymmetric
  • Progress to branches
  • Renal involvement common
  • HTN may develop
  • Skin lesions and motor weakness (wrist or foot drop)
  • No diagnostic lab test, diagnose by biopsy and ateriogram (will see microaneurysms and
    abrupt cut off)
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24
Q

Hepatitis D

A

ssRNA virus

  • Diagnosis — IgM and IgG antibodies, HDV, RNA serum
  • Transmission — parenteral
  • Incubation — 2-12 weeks
  • No vaccine
  • Prognosis poor when associated with HBV
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25
Q

For Hepatitis, it acute or chronic infection? Would you do elective dental work?

A

If acute, NO
 With pain, only do palliative treatment!
 Avoid acetaminophen
o If chronic, is it under control?
 Hard to know if it’s under control unless the patient does regular blood
work
 What about bleeding? Ask how long it takes to stop bleeding when they
get a cut to help determine if it’s controlled or not

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26
Q

Dental Management of patients with Hepatitis

A
  • Lab tests?
    o PT and PTT to assess bleeding/coagulation in patients with liver disease
    o Platelets will also help you tell if its alcoholic liver disease

Avoid anything that is metabolized in the liver or is difficult to metabolize such as antibiotics or pain meds.

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27
Q

Cancers with Metastasis in the Mandible

A

Liver cancer
Breast cancer
Prostate Cancer
Melanoma

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28
Q

Alcoholic Liver Disease

A

Etiology —alcohol ingestion

  • Unknown amount of alcohol that predicts the development of ADL
  • Other coexistent liver diseases
  • Cirrhosis — hepatic failure
  • Esophagitis, gastritis, generalized malnutrition
  • Weight loss and protein deficiency (coagulation factors)
  • Impairment of glucose metabolism
  • Renal failure
  • Portal hypertension
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29
Q

Clinical Presentation of Alcoholic Liver Disease

A 
Enlarged parotid glands
Spider angiomas
Jaundice 
Ascites 
Hematemesis 
Hepatomegaly
Splenomegaly 
Epigastric pain

Later stage –> thrombocytopenia and coagulation disorders.

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30
Q

Oral Complications of Alcoholic Liver Disease

A 
Poor oral hygiene
Oral neglect
Glossitis
Candidiasis
Gingival bleeding 
Petechiae 
Parotid enlargement
Impaired healing, Infections
Dental attrition 
Xerostomia
Oral cancer

o Alcohol causes problems with platelets, which can cause petechiae that is seen orally

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31
Q

Chronic Liver Disease

A

Vitamin K —important for coagulation factors II (prothrombin), VII, IX and X.

  • Fat soluble vitamin
  • Requires proper liver function to be absorbed by the intestines
  • In general, with chronic liver disease, we get problems with synthesis of coagulation
    factors, but also malabsorption
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32
Q

Child-Pugh score — Child-Turcotte-Pugh score or Child Criteria

A

Assess the prognosis of chronic liver disease, mainly cirrhosis

  • Look at level of bilirubin, serum albumin, PT or INR, ascites, and hepatic encephalopathy
  • Use these to do a simple classification of the level of severity of liver disease
  • Class A = 5-6 points, least severe liver disease
  • Class B = 7-9 points, moderately severe liver disease
  • Class C = 10-15 points, most severe liver disease
    o May not be a candidate for a transplant anymore because of high risk
33
Q

Compound in energy drinks that causes ACUTE Hepatitis (not viral)

A

NIACIN

save in pharmaceutical dose but can cause liver toxicity in excess

34
Q

L.A. Metabolized Primarily by the Liver

A

Lidocaine, Mepivacaine, Prilocaine, Bupivacaine

o Mepivacaine is second choice LA after Lidocaine, doesn’t have epinephrine
o Most of these agents appear to be safe for use in patients with liver disease
when given in appropriate amounts
 Generally shouldn’t use more than 3 carpules

35
Q

Analgesics Metabolized Primarily by the Liver

A

Acetaminophen, Codeine, Aspirin, Ibuprofen

Limit dose or avoid (only in severe cases)
o Acetaminophen can be taken for many different types of pain, which resulted in overuse and frequent hospitalization for liver disease in the past

o Max dose was reduced from 4000mg to 3000mg, and for most people we
recommend no more than 2000mg
o Also shouldn’t combine medications!

36
Q

Sedatives/Antibiotics Metabolized Primarily by the Liver

A

Sedatives —Diazepam (Valium), Barbiturates
- Antibiotics —Ampicillin, Metronidazole
o Amoxicillin with Metronidazole is often used to treat perio disease, but this is NOT ok for someone with liver disease

37
Q

Stellate Cells

A

Located in the Space of Disse
In its quiescent form, it is a lipid (vitamin A) storing cell

The principal cell type involved in generalized scar formation / deposition (acute and chronic)

Involved especially in alcoholic and non-alcoholic fatty liver disease

38
Q

Main Patterns of Hepatic Injury

A 
Degeneration and intracellular accumulation
 Necrosis and apoptosis
 Regeneration
 Inflammation
 Cirrhosis
 Ductular reaction
39
Q

Degeneration and intracellular accumulation

A

If moderate and the agent is removed, may be reversible
Due to toxic or immunologic factors
Accumulation of

  • fat droplets (steatosis)
  • copper
  • iron
  • bilirubin (cholestasis)

Appearance:

  • ballooning degeneration
  • single large droplet
  • multiple tiny droplets
EXAMPLES:
Alcoholic liver disease
 Acute fatty liver of pregnancy
 Wilson’s disease
Reye syndrome
40
Q

Reye syndrome

A

rare but serious condition

  • affects young children with viral illness
  • use of aspirin was linked with it (90% of cases)
  • hepatic fatty change + rapidly progressing encephalopathy
  • starts with rash on palms and soles, vomiting, confusion, lethargy
  • could be lethal or followed by mild to severe permanent brain damage
41
Q

Necrosis and apoptosis

A

Irreversible changes

Apoptosis
- Shrunken, pyknotic hepatocytes + Acidophilic (apoptotic) bodies

Necrosis

  • Cell membrane deterioration
  • Swelling and rupture of hepatocytes
  • Defective osmotic regulation
  • Accumulation of macrophages
42
Q

Types of necrosis

A
  • Coagulative necrosis – in ischemia
  • Hydropic degeneration – viral hepatitis
  • Focal necrosis – viral or drug-induced
  • Zonal necrosis (zone 1-3) –
  • Bridging necrosis – inflammation or toxic
  • Piecemeal necrosis – viral (chronic), autoimmune, steatohepatitis
  • Submassive necrosis
  • Massive necrosis
43
Q

Inflammation

A

Due to a wide array of factors (e.g. viral, toxins, drugs, autoimmune)
Acute or chronic
Necrosis of hepatocytes may precede or follow the inflammation
Periportal or into the parenchima of liver (zone 1)

44
Q

Regeneration

A

Under normal circumstances, very little liver proliferation

After liver injury (or resection), proliferation occurs as a compensation for tissue loss

Regeneration of lost hepatocytes occurs primarily by mitotic replication of hepatocytes adjacent to those that have died

Replicative senescence of hepatocytes may occur in time in chronic disease

Cells of the canals of Hering (oval cells) represent reserve progenitor cells for both hepatocytes and bile duct cells

45
Q

Ductular (ductal) reaction

A

Progenitor cells for bile duct cells. Most prominent in cirrhosis.

46
Q

Fibrosis

A

In response to inflammation or direct response to a toxic agent

Initially may develop portal, periportal, pericentral or pericellular

Later in time, bridging fibrosis

47
Q

Cirrhosis

A

Etiology

  • Alcohol abuse
  • Non-alcoholic fatty liver disease (NAFLD)
  • Chronic hepatitis B and C
  • Autoimmune hepatitis
  • Biliary disease
  • Metabolic disease
  • Cryptogenic (10% of cases)

Four pathological processes

1) Hepatocellular death
2) Vascular changes
3) Progressive fibrosis
4) Regeneration (nodules)

 Coexist in various degrees
 Affect diffusely the liver
 The hepatic architecture is disrupted
 Usually most changes are irreversible
 All liver functions are affected

Symptomatology
About 40% of patients are asymptomatic until the
advanced stages of the disease

Symptomatic patients:
- non-specific symptomatology
- symptoms and signs suggestive for cirrhosis
Laboratory tests
Abnormal results even in asymptomatic patients

 Complications
 Progressive (chronic) liver failure
 Portal hypertension (and risk of rupture of
esophageal varices)
 Hepatocellular carcinoma (HCC)
48
Q

Clinical Syndromes

A

HEPATIC FAILURE
CIRRHOSIS
PORTAL HYPERTENSION
CHOLESTASIS

49
Q

Three situations of heart failure

A

1) Acute liver failure with massive hepatic necrosis:
Rare but life-threatening
Fulminant (≤ 8 weeks) or subfulminant (≤ 26 weeks)
b/w onset and hepatic encephalopathy in the absence
of pre-existing liver disease
Massive hepatic necrosis (toxic or immune mediated)
Liver larger or smaller than normal
Caused by Acetaminophen (50% cases), Amanita phalloides, Autoimmune hepatitis, and Acute viral hepatitis

2) Chronic:
Progressive evolution of chronic liver disease that ends in cirrhosis

3) Hepatic dysfunction without overt necrosis:
Reye syndrome
Tetracycline toxicity
Acute fatty liver of pregnancy (diffuse microvesicular steatosis due to mitochondrial dysfunction) – third
trimester and early postpartum

50
Q

Hepatic encephalopathy

A

a disorder of neurotransmission in the central nervous
system and neuromuscular system.

Elevated ammonia levels in blood and the central nervous system correlate with impaired neuronal function and cerebral edema.

Encephalopathy may progress over days, weeks, or months following acute injury.

Pathophysiology
Severe loss of hepatocellular function
Shunting of blood from portal to systemic circulation leading to ammonia in the blood

Disturbances in consciousness, ranging from subtle behavioral abnormalities, to marked
confusion and stupor, to deep coma and death.

Asterixis IS A PARTICULAR SIGN!!**

51
Q

Acetaminophen-induced centrilobular necrosis

A

This is a zone 3 necrosis (accumulating effect)

Onset: first with nausea, vomiting, and often jaundice.
Later: encephalopathy, multisystem failure.
Liver initially enlarged, then it shrinks dramatically.
Serum liver transaminases are initially very elevated;
then decline (not a sign of improvement!).
Worsening jaundice.
Coagulation defects (low level of vitamin K)
Death occurs without liver transplantation.

52
Q

Hepato-renal syndrome

A

Renal failure without preexisting kidney condition (exceptions exist)
Liver and kidneys may be affected by same agents or processes
From mild to severe
Renal function promptly improves if hepatic functions improved
Decreased renal perfusion
Decreased glomerular filtration rate
Oliguria (although the ability to concentrate the urine is retained)
High levels of blood urea nitrogen and creatinine
Sodium retention
Ascites (refractory to diuretic therapy)
Impaired free-water excretion

53
Q

PORTAL HYPERTENSION

A

increased resistance in the portal blood flow

can have intrahepatic and posthepatic causes;
Intrahepatic include cirrohosis, nodular regeneration hyperplasia, malignancy, amyloidosis, etc.

Posthepatic causes include SEVERE RIGHT SIDED HEART FAILURE, constrictive percarditis, hepatic vein outlow obstruction

four major clinical consequences of portal hypertension are:

(1) hepatic encephalopathy
(2) portosystemic venous shunts
(3) ascites
(4) congestive splenomegaly

54
Q

Sites of porto-caval anastomoses

A

1) Distal third of esophagus (esophageal varices)
2) Rectum (internal hemorrhoids)
3) Paraumbilical area (caput medusae)
4) Retroperitoneum

55
Q

Metabolic Liver Disease

A

Acquired:
• Non alcoholic fatty liver disease

Inherited metabolic diseases:
• Hemochromatosis
• Wilson disease
• α1‐antitrypsin deficiency

56
Q

Hemochromatosis

A

Total iron is tightly regulated by intestinal absorption

Excessive accumulation of iron in the liver and pancreas
> Also heart, joints, adrenals, thyroid, skin

Primary or secondary
Secondary: Consequence of parenteral administration (blood transfusions), hemodialysis, sickle cell**

Neonatal (congenital):
• Unknown etiology
• Severe liver disease and extrahepatic deposition
• Liver injury in utero → hemosiderin accumulation
• May be related to maternal immune injury towards fetal liver

The adult form of hemochromatosis is almost always
caused by mutations of HFE gene

57
Q

Symptoms of Hemochromatosis

A

Symptoms usually first appear in the fifth to sixth
decades of life
• Male predominance (5‐7 : 1)
• Earlier clinical presentation in males
• Diagnosed by high levels of serum Iron and ferritin
• The classic triad might not develop until late in
the course of the disease
1. pigment cirrhosis with hepatomegaly
2. skin pigmentation
3. diabetes mellitus
• Death results from cirrhosis or cardiac disease
• Hepatocellular Ca: risk is 200‐fold than gen pop
• Treatment for Fe overload does not remove risk
• Treated by phlebotomy and iron removal

58
Q

Wilson Disease

A 
• Autosomal recessive disorder
• Impaired copper excretion into bile and failure to
incorporate copper into ceruloplasmin
• α‐2 globubin + Cu = Celuloplasmin
• Low ceruloplasmin levels in WD
• Accumulation of toxic levels of copper in many
organs, principally the
‐ liver
‐ brain
‐ eye

• Diagnosis based on:
• Decreased serum ceruloplasmin (Serum Cu may be
normal, increased or decreased)
• Increased Urinary excretion of Cu
• Increased hepatic content of Cu
• Kayser Fleischer rings
• Treatment: Long term Copper chelation with D‐
penicillamine or liver transplant (if cirrhosis)

59
Q

Symptoms of Wilson Disease

A 
Kayser Fleischer Rings in eyes 
Putamen atrophy / cavitation
Cirrhosis
Slurred speech 
Diminished movement control (tremors like Parkinsons) 
Mild behavior change
Frank psychosis
60
Q

Alpha‐1 Antitrypsin Deficiency

A

• Autosomal recessive disorder

• Liver derived AAT provides 90% of
elastase inhibition in plasma

  • Clinically:
  • Early onset emphysema (<45 y)
  • Unexplained liver disease w/ cirrhosis
61
Q

Changes in Bilirubin lead to what urine/feces color changes?

A

Prehepatic cause (hemolysis): dark feces and dark urine
Hepatic tissue damage: pale feces and dark urine
Posthepatic: clay colored feces (no color) and urine is pale

62
Q

Jaundice

A

The balance between bilirubin production and clearance is disturbed by one or more of the following mechanisms:

  1. Excessive extrahepatic production of bilirubin
  2. Reduced hepatocyte uptake
  3. Impaired conjugation
  4. Decreased hepatocellular excretion
  5. Impaired bile flow
  • *1, 2 & 3: Unconjugated hyperbilirubinemia
  • *4 & 5: Predominantly conjugated hyperbilirubinemia
63
Q

Hemolytic disease of the newborn

A

(erythroblastosis fetalis) may lead to accumulation of
unconjugated bilirubin in the brain
• Rh incompatibility
• May cause severe neurologic damage (kernicterus)

64
Q

Neonatal jaundice

A

mild unconjugated hyperbilirubinemia

Treatment: Phototherapy

• Works through isomerization that changes trans‐
bilirubin into water‐soluble cis‐bilirubin isomer

65
Q

Cholestasis

A

Impaired bile formation and bile flow →
accumulation of bile pigment in the liver parenchyma
• Extrahepatic or intrahepatic obstruction of bile channels
• Defects in hepatocyte bile secretion
• Clinical symptoms: Jaundice, pruritus, skin xanthomas (focal accumulation of cholesterol), intestinal malabsorption

• Characteristic lab finding:
• Elevated serum alkaline phosphatase and γ‐glutamyl
transpeptidase (GGT)
• Enzymes present on the apical membranes of hepatocytes and bile duct epithelial cells

66
Q

Intrahepatic Biliary Disease

A

Two entities:

1) Primary Biliary Cirrhosis (PBC)&raquo_space; issue starts in liver
2) Primary Sclerosing Cholangitis (PSC)&raquo_space; starts in liver and then there’s thickening and inflammation of the bile duct

67
Q

Primary Biliary Cirrhosis (PBC)

A
  • Inflammatory autoimmune mainly affecting medium‐sized intrahepatic bile ducts
  • Unknown pathogenesis
  • Portal inflammation, scarring, and eventual development of cirrhosis and liver failure (cirrhosis develops after many years)
  • Seen in middle age with a predominance in females and in conjunction with other autoimmune conditions
 Insidious onset
• Fatigue and pruritus
• Hepatomegaly
• Eyelid xanthelasmas / Hyperpigmentation
• Inflammatory arthropathy

• ↑ Serum alkaline phosphatase and cholesterol
• Antimitochondrial antibodies in 90% to 95% of
patients which is HIGHLY characteristic of PBC and ESSENTIAL for diagnosis

• Causes of death:
‐ liver failure
‐ massive variceal hemorrhage
‐ intercurrent infection

• Increased risk to develop hepatocellular carcinomas

68
Q

Primary Sclerosing Cholangitis (PSC)

A

• Characterized by inflammation and obliterative
fibrosis of intrahepatic and extrahepatic bile ducts,
with dilation of preserved segments

• Immunologically mediated injury to bile ducts

• Commonly seen in association with Inflammatory
bowel disease, particularly ulcerative colitis

•BEADING There’s alternating dilations and strictures, creating the appearance of beads that can be seen radiographically

•Concentric periductal fibrosis around affected
ducts (“onion‐skin fibrosis”)

69
Q

Cholelithiasis (gallstones)

A
  • 10% to 20% of adults in developed countries
  • > 80% are “silent”

• Two main types of gallstones
1) About 90% are cholesterol stones containing >50%
of crystalline cholesterol monohydrate
• Rest are pigment stones composed predominantly
of bilirubin calcium salts

pigmented stones are more common in Asia and cholesterol stones are commonly caused by oral contraceptives, rapid weight loss, and diet.

Biliary pain
• Can be excruciating and constant or “colicky” (spasmodic)
• Result of the obstruction
• Larger calculi are less likely to enter the cystic or common ducts to produce obstruction, small stones or “gravel” are more dangerous

70
Q

Cholesterol stones

A
  • Pure cholesterol stones are pale yellow, round to ovoid, have a finely granular, hard external surface
  • With increasing proportions of calcium carbonate, phosphates, and bilirubin, stones may be lamellated and gray‐white to black

• Surfaces of multiple stones may be rounded or faceted, because of tight
apposition

• Stones composed largely of cholesterol are radiolucent (However, sufficient calcium carbonate is found in 10% to 20% of cholesterol stones to render
them radiopaque)

71
Q

Pigmented stones

A
  • “Black” and “brown”
  • Black pigment stones are found in sterile gallbladder bile
  • Brown stones are found in infected intrahepatic or extrahepatic ducts

• Because of calcium carbonates and phosphates, approximately 50% to 75%
of black stones are radiopaque

• Brown stones, which contain calcium soaps, are radiolucent

72
Q

Cholecystitis

A

• Inflammation of the gallbladder
• May be acute, chronic, or acute superimposed
on chronic
• Almost always occurs in association with
gallstones
• Cholecystitis is one of the most common
indications for abdominal surgery in the US

73
Q

Acute Calculus Cholecystitis

A

An acute inflammation of the gallbladder, precipitated
90% of the time by obstruction of the neck or
cystic duct

• Primary complication of gallstones

• Chemical irritation and inflammation of the obstructed
gallbladder/ mucosal and mural inflammation

  • Gallbladder impaired mobility (porcelain gallbladder)
  • Distention and increased intraluminal pressure compromise blood flow to the mucosa
  • Absence of bacterial infection – Only later in the course may bacterial contamination develop
74
Q

Acute Acalculous Cholecystitis

A

• Thought to result from ischemia
• Cystic artery is an end artery (no collateral circulation)
• Occurs in patients who are hospitalized for
unrelated conditions

Risk factors:
• Sepsis with hypotension and multisystem organ failure
• Immunosuppression
• Major trauma and burns
• Diabetes mellitus
• Infections
75
Q

Liver Nodules and Tumors

A 
Nodular Hyperplasias
• Solitary or multiple hyperplastic liver nodules in
the non cirrhotic liver
• Focal nodular hyperplasia (FNH)
• Nodular regenerative hyperplasia (NRH)

Benign neoplasms
• Cavernous Hemangioma
• Hepatic adenoma

76
Q

Hepatocellular Carcinoma

A 
Four major etiologic factors:
• Chronic viral infection (HBV, HCV)
• Chronic alcoholism
• Non‐alcoholic steatohepatitis (NASH)
• Food contaminants (primarily aflatoxins)

Could be
‐ Unifocal: usually one large mass
‐ Multifocal: widely distributed nodules of variable size
‐ Diffusely infiltrative cancer: sometimes entire liver
• Well differentiated or poor differentiated forms
• Repeated cycles of cell death and regeneration (eg.
Chronic hepatitis)
• Liver enlargement
• The diffusely infiltrative tumor may blend imperceptibly into a cirrhotic liver background
• Pale tumors with green hue
• Vascular invasion
• Portal vein or inferior vena cava involvement
• Intrahepatic metastases
• Satellite nodules (shown by molecular methods to be
derived from the parent tumor)

• Metastases outside the liver are primarily via
vascular routes (lung, late in disease)
• Lymph node metastases to the perihilar, peripancreatic, and para‐aortic nodes above and
below the diaphragm

77
Q

Cholangiocarcinoma

A

Arising from bile ducts within and outside of the liver
• Risk factors
• Primary sclerosing cholangitis (PSC)
• HCV infection
• Previous exposure to Thorotrast (formerly used in
radiography of the biliary tract)
• In southeast Asia, chronic infection of the biliary tract by a liver fluke

78
Q

Intrahepatic and extrahepatic forms of Cholangiocarcinoma

A

• Extrahepatic (80 to 90% of the tumors)
• Perihilar tumors (Klatskin tumors) located at the junction of the
right and left hepatic ducts forming the common hepatic duct
• Symptoms of biliary obstruction, cholangitis, and right upper
quadrant pain
• Small at time of diagnosis
• Intrahepatic
• Usually detected late in their course
• Obstruction of bile flow or a symptomatic liver mass

Systemic Pathology (8 decks)

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