GI: Pancreas, Liver, Gallbladder Flashcards

1
Q
  • Developmental malformation in which the Pancreas forms a Ring around the Duodenum
  • Risk of Duodenal obstruction
  • Embryology tie-in w/ Head of Pancreas
A

Annular Pancreas

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2
Q
  • Inflammation and Hemorrhage of the Pancreas
  • Autodigestion of Pancreatic Parenchyma by Enzymes
  • Trypsin activates other Pancreatic enzymes
  • Liquefactive Hemorrhagic Necrosis and Fat Necrosis
  • A/w Alcohol (Sphincter of Oddi) and Gallstones
  • Trauma, Hypercalemia, Hyperlipidemia, Drugs, Scorpion Stings, Mumps, Rupture of a Posterior Duodenal Ulcer (Head of Pancreas sits posterior)
  • Pain radiates to the Back a ‘Boring
  • Nausea and Vomiting
  • Periumbilical and Flank Hemorrhage (Periumbilical soft tissue and Retroperitoneum)
  • Elevated Serum Lipase and Amylase
  • Phospholipase –> ARDS
  • Hypocalcemia w/ Saponification of Fat Necrosis
A

Acute Pancreatitis

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3
Q
  • Fibrosis of Pancreatic Parenchyma
  • 2nd to Recurrent Acute Pancreatitis
  • Alcohol (Adults) and Cystic fibrosis (Children);
    Most –> Idiopathic
  • Epigastric abdominal pain –> Radiates to the Back
  • Pancreatic insufficiency –> Results in Malabsorption w/ Steatorrhea and Fat-soluble Vit. Def. (ADEK)
  • Amylase and Lipase are not useful Serologic markers –> Destroyed
  • Dystrophic Calcification of Pancreatic Parenchyma on Imaging
  • Chain of Lakes’ pattern due to dilation of Pancreatic Ducts
  • 2nd to Diabetes Mellitus –> Late complication due to Destruction of Islets
  • Increased risk Pancreatic Carcinoma (Adenocarcinoma of Pancreatic ducts)
A

Chronic Pancreatitis

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4
Q
  • Adenocarcinoma arising from the Pancreatic Ducts
  • Elderly (avg. 70 y.o.), < 5% 5-year survival
  • Smoking and Chronic Pancreatitis
  • Epigastric Abdominal pain and Weight loss
  • Obstructive Jaundice w/ Pale stools and Palpable gallbladder, a/w Tumors that arise in the Head of the Pancreas
  • 2nd Diabetes Mellitus; a/w Tumors in Body or Tail of Pancreas
  • Pancreatitis
  • Migratory thrombophlebitis (Trousseau sign); Swelling, Erythema, Tenderness in extremities (10%)
  • Serum Tumor marker CA 19-9
  • Surgical en bloc of Head and Neck, proximal Dudenum, and Gallbladder –> Whipple procedure
  • -> 1 yr. survival < 10%
A

Pancreatic Carcinoma

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5
Q
  • Failure to form or early Destruction of Exrahepatic Biliary Tree –> No lumen
  • Leads to Biliary Obstruction w/in first 2 months of life
  • Jaundice and progresses to Cirrhosis –> Pale stool
A

Biliary Atresia

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6
Q
  • Solid, Round stones in Gallbladder
  • Precipitation of Cholesterol or Bilirubin in Bile
  • Supersaturation of Cholesterol or Bilirubin
  • Decreased Phospholipids (Solubilize cholesterol)(lecithin) or Bile acids
  • Stasis
  • RUQ pain, Nausea, Vomiting, Low-grade Fever, Leukocytosis
  • Gangrene of the Gallbladder, Peforation, Fistula, Bowel obstruction, etc…
  • Clofibrate – Lipid lowering agent used to control High Cholesterol
A

Cholelithiasis (Gallstones)

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7
Q
  • Radiolucent (10% are opaque), Cholesterol monohydrate
  • Age (40s), Estrogen (Female gender, Obesity, Multiple pregnancies, Oral contraceptives, Hormone replacement therapy
  • Fat, Female, Forty, Fertile, and Fucks (5 –F’s)
  • Clofibrate – lipid lowering agent used to control for High Cholesterol (Hmg)
  • Native American Pima and Navajo Indian ethnicity
  • Crohn disease – dmg to terminal ilieum –> decreased Bile reuptake –> increased cholesterol precipitation
  • Cirrhosisdecreased productionof Bile salts
A

Cholesterol Stones

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8
Q
  • Black pigmented Stones composed of Calcium salts and Unconjugated Bilirubin (UCB)
  • Radiopaque
  • A/w Chronic hemolytis anemias, Cirrhosis, Bacterial infection, and Parasites
  • A/w Extravascular Hemolysis (Reticular endothelial
    –> Splenic Macrophages –> Unconjugated bilirubin)(increased Bilirubin in bile) and Biliary tract infection
    (E coli, Ascaris lumbricoides, and Clonorchis sinensis)
A

Bilirubin Stones

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9
Q
  • Common Roundworm that infects 25% of the Worlds population, especially in areas w/ Poor sanitation (Fecal-oral transmission)
  • Infects the Biliary tract
  • Increases risk for Gallstones
A

Ascaris lumbricoides

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10
Q
  • Endemic in China, Korea, and Vietnam (Chinese Liver flukes)
  • Infects the Biliary tract
  • Increases the risk of Gallstones
  • Cholangitis
  • Cholangiocarcinoma
A

Clonorchis sinensis

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11
Q
  • Waxing and Waning RUQ Pain
  • Gallbladder contracting against a Stone lodged in the Cystic duct
  • Symptoms relived when Stone passes
  • Common Bile duct obstruction may result in
  • *Acute Pancreatitis** or Obstructive Jaundice
A

Biliary Colic

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12
Q
  • Acute Inflammation of the Gallbladder wall
  • -> squeezes blood vessels –> Ischemia
  • Impacted stone in Cystic duct
  • -> Dilation w/ Pressure ischemia
  • Bacterial overgrowth (E coli)
  • Inflammation and Bloating
  • RUQ Pain –> Radiating to Right Scapula, Fever w/ increased WBC count, Nausea, Vomiting, and increased Serum Alkaline Phosphatase (Duct dmg)
  • Risk of rupture if left untreated
A

Acute Cholecystitis

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13
Q
  • Chronic inflammation of Gallbladder
  • Chemical irritation from Longstanding cholelithiasis w/ or w/out Superimposed bouts of Acute cholecystitis
  • A/w Herniation of Gallbladder mucosa into Muscular Wall (Rokitansky-Aschoff sinuses)
  • Vague RUQ Pain, Postprandyl pain
  • Porcelain Gallbladder is a late complication – Shrunken, Hard Gallbladder due to Chronic Inflammation, Fibrosis, and Dystrophic Calcification
  • Increased risk for Carcinoma
  • Tx: Coholecystectomy, esp. w/ Porcelain Gallbladder
A

Chronic Cholecystitis

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14
Q
  • Bacterial infection of the Bile ducts
  • A/w Ascending infection w/ Enteric Gram-Negative bacteria
  • Presents as Sepsis (High Fever and Chills), Jaundice, and Abdominal Pain
  • Increased incidence w/ Choledocholithiasis (stone in Biliary duct –> decreases flow washout)
  • Triad: Epigastric / RUQ pain, Fever, and Jaundice
A

Ascending Cholangitis

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15
Q
  • Gallstone enters and Obstructs the Small Bowel
  • Due to Cholecystitis w/ Fistula formation between the Gallbladder and Small Bowel
A

Gallstone Ileus

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16
Q
  • Adenocarcinoma arising from the Glandular epithelium that lines the Gallbladder-wall
  • Gallstones are a Major risk factor, esp. w/ Porcelain Gallbladder
  • Clonorchis sinensis (Liver Flukes)
  • Cholecystitis in an Elderly Woman (40 – 70 y.o.)
  • -> Gallbladder Carcinoma –> Poor prognosis
  • Klatskin tumor - carcinoma of the Bifurcation of the Right and Left Hepatic Bile ducts
A

Gallbladder Carcinoma

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17
Q
  • Yellow discoloration of the Skin and Scleral Icterus
  • Increased Serum Bilirubin > 2.5 mg/dL
  • A/w Bilirubin metabolism disturbance
A

Jaundice

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18
Q
  • High lvls of UCB overwhelm the conjugating ability of the Liver
  • Increased UCB (not water soluble)
  • Dark urine due to increased urine Urobilinogen, increased Conjugated-UCB
  • Increased Risk for Pigmented Bilirubin Gallstones
A

Extravascular Hemolysis
or
Ineffective Erythropoiesis

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19
Q
  • Newborn Liver has transiently low UGT activity (UGT1A1 activity, decreased excretion)
  • Increased UCB –> Fat soluble –> Depositions in Basal Ganglia of the Brain (Kernicterus) –> Neurological deficits and Death
  • Tx: Phototherapy (makes UCB water soluble) –> urinate out Bilirubin
A

Physiologic Jaundice of the Newborn

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20
Q
  • Mildly low UGT activity (UGT1A1)
    (UDP-glucuronosyltransferase deficiency)
  • Autosomal recessive
  • Increased UCB
  • Diffuse Hepatocellular disease
  • Jaundice during stress (e.g. Fasting, Severe Infection); otherwise not clinically significant
A

Gilbert Syndrome

21
Q
  • Absence of UGT (severe)
    (Deficiency of UGT1A1 activity)
    –> Unconjugated hyperbilirubinemia
  • Increased UCB
  • Type I - Kernicterus - Usually fatal - Autosomal recessive - Fatal in Neonatal period
  • Type II - Jaundice - Autosomal Dominant w/ variable penetrance - Generally mild, occasional Kernicterus
A

Crigler-Najjar Syndrome

22
Q
  • Deficiency of Bilirubin Canalicular ABC transport protein (cMOAT)
  • Impaired biliary excretion of bilirubin glucouroides due to Mutation in Multiple Drug-resistant Protein 2 (MRP2) –> Pigmented Cytoplasmic Globules ‘BLACK’
  • Benign Autosomal recessive
  • Increased CB (Conjugated Hyperbilirubinemia)
  • Normal AST and ALT
  • No Clinical Consequences
  • The Liver is dark; otherwise, not clinically significant –> ‘Pitch Black Liver’ ‘Pitch Dark’ – Gallbladder cannot be visualized
  • Similar to Rotor Syndrome –-> Normal appearance, Gallbladder can be visualized
A

Dubin-Johnson Syndrome

23
Q
  • A/w Gallstones, Pancreatic Carcinoma, Cholangiocarcinoma, Parasites, and Liver Fluke (Clonorchis sinensis)
  • Increased CB
  • Decreased Urine Urobilinogen
  • Increased Alkaline phosphatase
  • Dark urine (Bilirubinuria) and Pale stool
  • Pruritus due to increased Plasma bile acids
  • Hypercholesterolemia w/ Xanthomas
  • Steatorrhea w/ Malabsorption of Fat-soluble vit. (ADEK)
A

Biliary Tract Obstruction

(Obstructive Jaundice)

24
Q
  • Inflammation disrupts Hepatocytes and Small Bile Ductules
  • Increased in Both CB and UCB
  • Increased AST and ALT
  • Dark urine due to increased Urine Bilirubine
  • Urine Urobilinogen is normal or decreased
A

Viral Hepatitis

25
Q
  • Fecal-oral transmission
  • Herpesvirus naked capsid RNA
  • HAV is commonly acquired by Travelers - ‘Infectious’
  • HEV is commonly acquired from Contaminated water or Undercooked seafood - ‘Enteric’
  • Acute Hepatitis; No Chronic state
  • Anti-virus IgM marks active Infection
  • Anti-virus IgG is protective, and its presence indicates prior infection or immunization (HAV only)
  • HEV infection in Pregnant Women is a/w Fulminant Hepatitis (Liver Failure w/ Massive Liver Necrosis)
A

Hepatitis A (HAV) and Hepatitis E (HEV)

26
Q
  • Serum’
  • Hepadnavirus enveloped DNA
  • Parenteral transmission (Childbirth, Unprotected intercourse, Intravenous Drug Abuse [IVDA], and Needle stick)
  • ‘Ground glass’ Hepatocytes (due to cytoplasmic HBsAg)
  • Results in Acute Hepatitis
  • Chronic disease occurs in 20% of cases –> a long-term risk of Hepatocellular carcinoma in pts. infected w/ HBV.
  • Vaccine
A

Hepatitis B (HBV)

27
Q

HBV Acute Stage

A
  • Increase HBsAG (Hepatitis B surface marker antigen)
  • Increase HBeAG and HBV DNA (envelope Antigen Transmission)
  • IgM – HBcAB – core Acute Battle
28
Q

HBV Window Stage

A
  • IgM – HBcAB – core Acute Battle
29
Q

HBV Resolved Stage

A
  • IgG – HBcAB – core Acute Battle
  • IgG – HBsAB – surface Acute Battle (protective)
30
Q

HBV Chronic Stage

A
  • Increase HBsAG (> 6 months)
  • +/- HBeAG and HBV DNA indicates infectivity
  • IgG – HBcAB – core Acute Battle
31
Q

HBV Immunization Stage

A
  • IgG – HBsAB – surface Acute Battle (protective)
32
Q
  • ‘Post-transfusion’ and ‘non-A, non-B’
  • Flavivirus enveloped RNA
  • Parenteral transmission (IVDA, Unprotected intercourse)
  • Risk from transfusion is almost nonexistent due to screening of the blood supply
  • Results in Acute hepatitis; Chronic disease occurs in most cases –> ‘Necrosis w/ portal bridging’
  • HCV-RNA test confirms infection ELISA
  • Decreased RNA levels indicate recovery
  • Persistence indicates Chronic disease
A

Hepatitis C (HCV)

33
Q
  • ‘Delta’
  • Defective enveloped circular RNA
  • Dependent on HBV for infection
  • Superinfection upon existing HBV is more severe than Coinfection (Infection w/ HBV and HDV at the same time)
  • Dx: Anti-HDV ELISA
A

Hepatitis D (HDV)

34
Q
  • End-stage liver damage
  • -> Disruption of Normal Hepatic parenchyma
  • Bands of Fibrosis and Regenerative nodules of Hepatocytes
  • Prothrombin time (PT) assess coagulopathy due to Liver disease
  • Fibrosis is mediated by TGF-β; from Stellate cells which lie beneath the endothelial cells that line the Sinusoids
  • Portal Hypertension leads to Ascites (fluid), Congestive Splenomegaly / Hypersplenism (consume RBCs and Platelets) and Portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae) and Hepatorenal syndrome (rapidly developing Renal failure secondary to Cirrhosis)
  • Decreased detoxification results in Mental status change, Asterixis, Coma
  • Gynocomastia, Spider angiomata and Palmar erythema due to Hyperestrinism
  • Jaundice
  • Decreased Protein Synthesis leads to Hypoalbuminea w/ Edema and Coagulopathy due to decreased clotting factors
A

Cirrhosis

35
Q
  • Dmg to Hepatic Parenchyma
  • Fatty Liver – accumulation of Fat in Hepatocytes (Steatosis)
  • Heavy and Greasy Liver
  • Alcoholic Hepatitis results from Chemical injury to Hepatocytes (Binge)
  • Acetaldehyde mediates dmg
  • Swelling of Hepatocytes w/ formation of Mallory bodies (dmg to cytokeratin intermediate filaments), Neutrophils, Fatty change, necrosis and acute inflammation
  • Fibrosis around the Central vein
  • Painful Hepatomegaly w/ (AST > ALT)
  • May result in Death
A

Alcohol-Related Liver Disease

36
Q
  • Fatty change, Hepatitis, and/or Cirrhosis that develop w/out Exposure to Alcohol or other known insult
  • A/w Obesity, Hyperinsulinemia, Insulin resistance, Type 2 Diabetes mellitus
  • Lipid accumulation in Hepatocytes
  • -> Steatohepatitis –> Cirrhosis
  • M = F
  • Diagnosis of exclusion; ALT > AST
A

Nonalcoholic Fatty Liver Disease

37
Q
  • Excess body Iron (Fe) leading to deposition in tissues and Organ dmg, HFE, HJV, TFR1, TFR2
  • Tissue dmg is mediated by Generation of Free Radicals
  • -> Fenton Rxn –> Heart, Pancreas, and Liver
  • Autosomal Recessive defect in Iron absorption (primary) or Chronic transfusions (secondary)
  • Primary Hemochromatosis mutations in HFE, gene, usually Chrom 6p21.3 - C282Y –> Increases small intestine absorption of Fe
  • Cysteine replaced by Tyrosine at AA 282
  • Triad: Cirrhosis, 2nd Diabetes Mellitus, Bronze skin
  • Dilated Cardiobyopathy, Cardiac Arrhythmias, Gonadal dysfunction (atrophy)
  • 5x M > F, Common among Northern European descent
  • Brown pigment in Hepatocytes
  • Increased risk of Hepatocellular carcinoma
  • -> Free radicals –> Dmg DNA
  • Tx: Phlebotomy and Chelating agents (Deferoxamine)
A

Hemochromatosis

  • Hemosiderosis = Acquired disorder of Fe overload due to repeated blood transfusions in pts. w/ Thalassemia
  • Hemochromatosis = Inherited disorder
38
Q
  • Hepatolenticular degeneration –> genetic disorder
  • Autosomal recessive defect (chrom 13q14.3 ATP7B gene)
  • -> P-type ATPase - ATP-mediated hepatocyte Copper transport into Bile and Ceruloplasmin
  • Lack of Copper transport into Bile
  • Lack of Copper incorporation into Ceruloplasmin – carries copper in Blood
  • Copper builds up in Hepatocytes, Leaks into Serum, Deposits in Tissues
  • Copper-production of Hydroxyl Free Radicals
  • -> Tissue Damage
  • Childhood or Adolescence cirrhosis (Liver disease)
  • Neurologic manifistations (Behavior, Dementia, Chorea, Parkinsonian)
  • Kayser-Fleisher rings in the Cornea
  • Increased Urinary Copper
  • Increased Hepatocellular carcinoma
  • Tx: D-penicillamine (chelates copper)
A

Wilson Disease

39
Q
  • Autoimmune Granulomatous destruction of Intrahepatic Bile Ducts
  • Women (avg. age is 40 y.o., 35 - 65 y.o’s)
  • 10x Females > Males
  • A/w other Autoimmune diseases (Sjogren Syndrome (70%), Scleroderma (5%), Typhoid disease (20%) Rheumatoid arthritis or SLE)
  • Unknown etiology
  • Antimitochondrial autoantibodies (AMA) (90%) are present - AMA + ANA + ANCA
  • Obstructive jaundice - Florid duct lesions and Loss of Small ducts
  • Pruritus, Xanthomas, Xanthelasmas, Serum Cholesterol, Fatigue
  • Cirrhosis is a late complication
A

Primary Biliary Cirrhosis

40
Q
  • Segmental Inflammation and Fibrosis of Intrahepatic and Extrahepatic Bile Ducts
  • Periductal Fibrosis w/ ‘onion-skin’ appearance: Concentric Fibrosis around Bile ducts and Segmental stenosis of Bile ducts w/ Bending and Strictures
  • Uninvolved regions are dilated resulting in a
    Beaded appearance’ of Bile duct
  • A/w Ulcerative colitis, IBD (70%), Pancreatitis, Fibrosing disease (Retroperitoneal diseases)
  • Males (70%) w/ 20 - 40 y.o’s
  • Unknown etiology; a/w Ulcerative Colitis and p-ANCA
  • Obstructive jaundice, and late Cirrhosis
  • Increased risk for Cholangiocarcinoma
A

Primary Sclerosing Cholangitis

41
Q
  • Fulminant Liver failure and Encephalopathy in Children w/ Viral illness w/ take Aspirin
  • Varicella or Influenza
  • Likely related to Mitochondrial dmg of Hepatocytes
  • Hypoglycemia
  • Elevated Liver enzymes
  • Causes Hepatic Fatty change (microvesicular steatosis) and Cerebral edema / Encephalopathy
  • Nausea and Vomiting –> Coma and Death
A

Reye Syndrome

42
Q
  • Benign Tumor of Hepatocytes (Liver cell adenoma)
  • A/w Oral contraceptive / anabolic steroids and Type I glycogen storage disease, in Young Women
  • Regress upon cessation of Oral contraceptive drugs
  • Microscopically tissue resembles normal Liver but lack of Portal tracts No Kupffer cells
  • Risk of Rupture and Intraperitoneal bleeding, especially during Pregnancy
  • Tumors are Subcapsular and Grow w/ Exposure to Estrogen
A

Hepatic Adenoma

43
Q
  • Malignant tumor of Hepatocytes (Asia, Japan, and sub-Saharan Africa)
  • “Eosinophilic Hepatocytes” w/ non-cirrhotic liver and fibrous collagen bundles
  • Chronic Hepatitis (HBV and HCV), and 4x Male > Female
  • Cirrhosis (Alcohol, Nonalcoholic Fatty Liver disease, Hemochromatosis, Wilson disease, and A1AT deficiency)
  • Aflatoxin B1 derived from Aspergillus (induced p53 mutations) - β-Catenin - a/w APC
  • Increased risk for Budd-Chiari syndrome
  • Liver infarction secondary to Hepatic vein obstruction
  • Painful Hepatomegaly and Ascites RUQ
  • Tumors often detected Late –> masked by Cirrhosis; poor prognosis, Increased AST and ALT
  • Serum Tumor marker is α-fetoprotein
A

Hepatocellular Carcinoma

44
Q
  • More common than primary liver tumors
  • Multiple well circumscribed masses
  • Detected as Hepatomegaly w/ nodular Free edge of the Liver
  • Colon
  • Stomach
  • Pancreas
  • Breast
  • Lung
  • Metastatic Melanoma
A

Metastasis to Liver

45
Q
  • Accumulation of Cholesterol-laden Macrophages w/in the Mucosa of the Gallbladder wall
  • Yellow speckling of the Red-tan mucosa - “Strawberry gallbladder”
  • Liped-laden Macrophages w/in Lamina Propria
A

Cholesterolosis

46
Q
  • Recent immigrants from Mexico, South America, India, etc.
  • Entamoeba histolytica
  • Necrotic abscess filled w/ Brown Pastelike Material ‘Anchovy paste’
  • Tx: ABX w/ or w/out Surgical drainage
A

Amebic Liver Abscess

47
Q
  • Most common genetic disease requiring Liver transplantation in Children
  • Autosomal recessive disorder of Protein folding
  • Production of α-1-AT produced by Pi gene (chrom 14) accumulates in Hepatocytes –> Liver damage
  • Inhibition of Proteases; Neutrophil elastase, Cathepsin G, and Proteinase 3 –> Pulmonary Emphysema
  • PiS (mild varient)
  • PiZ (markedly reduced levels)
  • PiZZ (severly reduced levels)
  • Micronodular cirrhosis w/ increased risk of Hepatocellular carcinoma and Panacinar emphysema (lungs)
  • PAS positive, Eosinophilic cytoplasmic globules w/in Hepatocytes - Round - Oval Cytoplasmic Globular inclusions in Hepatocytes
  • Tx: Smoking cessation and Liver Transplantation
A

α-1-Antitrypsin Deficiency

48
Q
  • Hepatic vein Thrombosis - occlusion of Two or more Hepatic veins by a Thrombus –> Hemodynamic Liver Disease –> Pain and Ascities
  • A/w predisposing for Thrombosis; Polycythemia vera, Pregnancy, Oral contraceptives, Paroxysmal Nocturnal hemoglobinuria, or Hepatocellular carcinoma
  • Abdominal pain, Hepatomegaly, Ascites, and Death
  • Microscopic Centrilobular Congestion and Necrosis
A

Budd-Chiari Syndrome

49
Q
  • Asymptomatic
  • Solid tumor in the Right lobe of the Liver
  • Consiting of a Fibrous core w/ Stellate projections
  • NOT a/w use of Oral contraceptives
  • Contains Biliary epithelium and Kupffer cells (Technetium scans show uptake)
A

Focal Nodular Hyperplasia