Hepatobilliary Pathology Flashcards

Question

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

Answer 1

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

Answer 2

- 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.

Answer 3

Liver cancer Breast cancer Prostate Cancer Melanoma

Answer 4

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

Answer 5

``` Enlarged parotid glands Spider angiomas Jaundice Ascites Hematemesis Hepatomegaly Splenomegaly Epigastric pain ``` Later stage --> thrombocytopenia and coagulation disorders.

Answer 6

``` 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

Answer 7

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

Answer 8

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

Answer 9

NIACIN | save in pharmaceutical dose but can cause liver toxicity in excess

Answer 10

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

Answer 11

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!

Answer 12

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

Answer 13

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

Answer 14

``` Degeneration and intracellular accumulation Necrosis and apoptosis Regeneration Inflammation Cirrhosis Ductular reaction ```

Answer 15

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 ```

Answer 16

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

Answer 17

Irreversible changes Apoptosis - Shrunken, pyknotic hepatocytes + Acidophilic (apoptotic) bodies Necrosis - Cell membrane deterioration - Swelling and rupture of hepatocytes - Defective osmotic regulation - Accumulation of macrophages

Answer 18

* 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

Answer 19

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)

Answer 20

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

Answer 21

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

Answer 22

In response to inflammation or direct response to a toxic agent Initially may develop portal, periportal, pericentral or pericellular Later in time, bridging fibrosis

Answer 23

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) ```

Answer 24

HEPATIC FAILURE CIRRHOSIS PORTAL HYPERTENSION CHOLESTASIS

Answer 25

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

Answer 26

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!!**

Answer 27

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.

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

Acquired: • Non alcoholic fatty liver disease Inherited metabolic diseases: • Hemochromatosis • Wilson disease • α1‐antitrypsin deficiency

Answer 32

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

Answer 33

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

Answer 34

``` • 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)

Answer 35

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

Answer 36

• Autosomal recessive disorder • Liver derived AAT provides 90% of elastase inhibition in plasma * Clinically: * Early onset emphysema (<45 y) * Unexplained liver disease w/ cirrhosis

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

mild unconjugated hyperbilirubinemia Treatment: Phototherapy • Works through isomerization that changes trans‐ bilirubin into water‐soluble cis‐bilirubin isomer

Answer 41

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

Answer 42

Two entities: 1) Primary Biliary Cirrhosis (PBC) >> issue starts in liver 2) Primary Sclerosing Cholangitis (PSC) >> starts in liver and then there's thickening and inflammation of the bile duct

Answer 43

* 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

Answer 44

• 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”)

Answer 45

* 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

Answer 46

* 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)

Answer 47

* “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

Answer 48

• 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

Answer 49

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

Answer 50

• 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 ```

Answer 51

``` 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

Answer 52

``` 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

Answer 53

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

Answer 54

• 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

Hepatobilliary Pathology Flashcards

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