Lecture 15 - Gastrointestinal Pathology II

Question 1

Atresias

Answer 1

• a congenital abnormality
• failure of development of intestinal lumen
• causes stenosis and obstruction (organ system was developing normal but then a portion disappears)
• most commonly the small intestine

Question 2

Meckel Diverticulum

Answer 2

• a congenital abnormality
• failure of involution of the omphalomesenteric duct
• leaves lung diverticulum usually in the ileum
  Complications:
• bacterial overgrowth depleting Vitamin B12 = pernicious anemia
• heterotopic tissue - pancreas/gastric mucosa w. ulceration

Question 3

Omphalocele

Answer 3

• congenital abnormality
• defect of umbilical musculature (weakens)
• creates sac into which intestines herniate

Question 4

Hirschsprung disease

Answer 4

• congenital megacolon
• caused by arrest of migration of neural crest cells
• do not distribute to anus
• creates aganglionic segment
• leads to marked dilatation of that segment (due to build up of fecal matter because abnormal peristalsis)

Question 5

Hepatitis

Answer 5

• inflammation of the liver

- most commonly caused by virus

Question 6

Hepatitis A

Answer 6

• “infectious hepatitis”
• benign, self-limited disease
  Transmission: fecal to oral
  Clinically: rarely fulminant (deadly) disease and doesn’t lead to chronic liver disease

Question 7

Hepatitis B

Answer 7

Transmission: infected blood/body fluids
5 clinical scenarios:
1. Acute hepatitis with recovery and clearance of virus (most common)
2. Nonprogressive chronic hepatitis (low inflammation of liver = won’t scar)
3. Progressive chronic disease ending in liver failure (due to scarring)
4. Fulminant hepatitis w. liver necrosis (=death)
5. Asymptomatic carrier state

Question 8

Hepatitis C

Answer 8

Transmission: most via blood; IV drug abuse accounts for >40%; blood transfusions were major cause in past.
Clinically:
- acute phase often asymptomatic
- Much higher rate of progression to chronic liver disease than HBV
- Most common cause of liver transplants in US
- Most have persistent infection
- Approximately 20% go on to liver failure

Question 9

Hepatic steatosis

Answer 9

• a change seen in alcohol liver damage
• Progressive accumulation of lipids (fat)
• Starts in centrilobular areas that progresses to larger accumulations
• Reversible until scarring occurs
• Grossly presents as enlarged “fatty liver”

Question 10

Cirrhosis

Answer 10

• Diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules
• bands of scar tissue that form around liver and into each other

Question 11

Ascites

Answer 11

• accumulation of peritoneal fluid
• a consequence of portal hypertension
• dilation increases venous pressure into the peritoneal

Question 12

Caput medusae

Answer 12

• dilation of superficial veins on skin
• formation of portosystemic shunt
• a consequence of portal hypertension
  (looks like medusa’s head)

Question 13

Asterixis

Answer 13

• tremors of head and extremities from a build up of toxins in the blood stream
• seen in hepatic encephalopathy - a major consequence of portal hypertension

Question 14

Hemachromatosis

Answer 14

• inherited metabolic disease
• genetic disorder
• Results in excessive accumulation of iron – deposited in parenchymal organs including liver and pancreas
• Develop pigmentation and iron deposition in other organs as well

Question 15

Wilsons Disease

Answer 15

• genetic disorder
• defect in copper metabolism
• can proceed to brain involvement (accumulate in brain)