Cirrhosis: Pathology review


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Cirrhosis: Pathology review

Gastrointestinal system

Peritoneum and peritoneal cavity disorders



Upper gastrointestinal tract disorders

Cleft lip and palate

Congenital diaphragmatic hernia

Esophageal web

Tracheoesophageal fistula

Pyloric stenosis



Oral candidiasis

Ludwig angina

Aphthous ulcers

Temporomandibular joint dysfunction

Dental abscess

Gingivitis and periodontitis

Dental caries disease

Oral cancer

Warthin tumor

Barrett esophagus


Plummer-Vinson syndrome

Mallory-Weiss syndrome

Boerhaave syndrome

Gastroesophageal reflux disease (GERD)

Zenker diverticulum

Diffuse esophageal spasm

Esophageal cancer

Eosinophilic esophagitis (NORD)


Gastric dumping syndrome

Peptic ulcer


Cyclic vomiting syndrome


Gastric cancer

Lower gastrointestinal tract disorders


Imperforate anus


Meckel diverticulum

Intestinal atresia

Hirschsprung disease

Intestinal malrotation

Necrotizing enterocolitis


Tropical sprue

Small bowel bacterial overgrowth syndrome

Celiac disease

Short bowel syndrome (NORD)

Lactose intolerance

Whipple's disease

Protein losing enteropathy

Microscopic colitis

Crohn disease

Ulcerative colitis

Bowel obstruction

Intestinal adhesions


Gallstone ileus

Abdominal hernias

Femoral hernia

Inguinal hernia

Small bowel ischemia and infarction

Ischemic colitis

Familial adenomatous polyposis

Peutz-Jeghers syndrome

Gardner syndrome

Juvenile polyposis syndrome

Colorectal polyps

Colorectal cancer

Carcinoid syndrome

Irritable bowel syndrome


Diverticulosis and diverticulitis


Anal fissure

Anal fistula


Rectal prolapse

Liver, gallbladder and pancreas disorders

Crigler-Najjar syndrome

Biliary atresia

Gilbert's syndrome

Dubin-Johnson syndrome

Rotor syndrome



Portal hypertension

Hepatic encephalopathy


Wilson disease

Budd-Chiari syndrome

Non-alcoholic fatty liver disease

Cholestatic liver disease

Hepatocellular adenoma

Autoimmune hepatitis

Alcohol-induced liver disease

Alpha 1-antitrypsin deficiency

Primary biliary cirrhosis

Primary sclerosing cholangitis


Neonatal hepatitis

Reye syndrome

Benign liver tumors

Hepatocellular carcinoma


Biliary colic

Acute cholecystitis

Ascending cholangitis

Chronic cholecystitis

Gallstone ileus

Gallbladder cancer


Acute pancreatitis

Pancreatic pseudocyst

Chronic pancreatitis

Pancreatic cancer

Pancreatic neuroendocrine neoplasms

Zollinger-Ellison syndrome

Gastrointestinal system pathology review

Congenital gastrointestinal disorders: Pathology review

Esophageal disorders: Pathology review

GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review

Inflammatory bowel disease: Pathology review

Malabsorption syndromes: Pathology review

Diverticular disease: Pathology review

Appendicitis: Pathology review

Gastrointestinal bleeding: Pathology review

Colorectal polyps and cancer: Pathology review

Neuroendocrine tumors of the gastrointestinal system: Pathology review

Pancreatitis: Pathology review

Gallbladder disorders: Pathology review

Jaundice: Pathology review

Viral hepatitis: Pathology review

Cirrhosis: Pathology review


Cirrhosis: Pathology review

USMLE® Step 1 questions

0 / 16 complete


USMLE® Step 1 style questions USMLE

of complete

A 67-year-old man comes to the clinic due to worsening fatigue and abdominal distension. The patient has lost 11 pounds in the last 2 months with minimal change in appetite. Past medical history is notable for chronic liver disease due to hepatitis B infection that was diagnosed 15 years ago. His most recent colonoscopy 1 year ago showed no abnormalities. His temperature is 37.0°C (98.6°F), pulse is 85/min, and blood pressure is 154/89 mm Hg. Physical examination reveals temporal wasting and scleral icterus. Palmar erythema and multiple spider angiomas are present. The abdomen is distended with shifting dullness to percussion. There is 2+ pitting edema of the lower extremities. Ultrasound shows a single homogenous liver mass with irregular borders. Which of the following best describes the tumor marker that is likely elevated in this patient?


Content Reviewers

Yifan Xiao, MD


Antonia Syrnioti, MD

Sam Gillespie, BSc

Ursula Florjanczyk, MScBMC

At the family medicine clinic, a 52- year- old male immigrant from Africa, named Jamar, came in for a checkup for the first time in a decade. On questioning, he admits to an extensive history of alcohol abuse. Physical examination reveals gynecomastia, palmar erythema and spider angiomata, as well as a palpable spleen.

Next, a 70- year- old Caucasian female, named Eleanor, with a history of chronic hepatitis C infection, is brought to the emergency department by paramedics due to altered mental status. She is completely disoriented and unable to provide an adequate history. Neurologic examination also reveals asterixis.

Lab tests of both show increased aspartate aminotransferase, or AST, and alanine aminotransferase or ALT. There’s also decreased albumin and increased prothrombin time. The difference is that Jamar has an AST level twice as high as ALT, in contrast with Eleanor, who has an ALT higher than AST. Eleanor, in particular, also has high serum levels of ammonia.

Both Jamar and Eleanor have cirrhosis. This is when chronic inflammation damages the liver causing it to become fibrotic. Normally, the liver is highly regenerative but scar tissue can replace liver cells which prevents regeneration and when this goes on for too long, it reaches the point where the damage is no longer reversible. If enough of the liver is replaced by scar tissue in advanced cirrhosis, a liver transplant might be needed. . Now, if we zoom into a hepatic lobule, we can see that it’s made of sheets of hepatocytes with sinusoids between them. The sinusoids are made of branches of the portal vein and hepatic artery, and together with the bile duct, form the portal triad which runs towards the central vein.

Now, there’s a space around each sinusoid, called the perisinusoidal space which contains stellate cells. When the hepatocytes are injured, they cluster together and form regenerative nodules. Here, they secrete paracrine factors that activate the stellate cells, which then proliferate, and start secreting transforming growth factor beta1, or TGF-beta. This causes them to produce collagen. The collagen builds up around the nodules and helps form scar tissue, leading to fibrosis.


  1. "Fundamentals of Pathology" H.A. Sattar (2017)
  2. "Robbins Basic Pathology" Elsevier (2017)
  3. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  4. "The Immunobiology and Pathophysiology of Primary Biliary Cirrhosis" Annual Review of Pathology: Mechanisms of Disease (2013)
  5. "Epidemiology of Alcoholic Liver Disease" Seminars in Liver Disease (2004)
  6. "Pathogenesis, Diagnosis, and Treatment of Alcoholic Liver Disease" Mayo Clinic Proceedings (2001)
  7. "Current concepts in the assessment and treatment of Hepatic Encephalopathy" QJM (2009)
  8. "Oxidative Stress and Epigenetic Instability in Human Hepatocarcinogenesis" Digestive Diseases (2013)
  9. "Involvement of DNA Damage Response Pathways in Hepatocellular Carcinoma" BioMed Research International (2014)
  10. "Hereditary Hemochromatosis — A New Look at an Old Disease" New England Journal of Medicine (2004)

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