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Flashcards in GI pathology Deck (30):

What is the most common congenital abnormality of the GI tract?

Imperforate anus.


Discuss the "rule of twos" with regards Meckel Diverticulum.

Meckels is a true diverticulum (involves all layers of the mucosa):

  • occurs in approx 2% of the pop'n
  • 2x as common in males
  • occurs within 2feet of the ileocaecal valve
  • usually approx 2cm long
  • usually asymptomatic by age 2yrs


What is another name for Hirschsprung Disease.

Also known as congenital aganglionic megacolon.


What is the pathogenesis of Hirschsprung disease?

A section of bowel lacks innervation -> aganglionosis. 

The bowel is unable to undergo peristalsis -> constipation -> functional obstruction -> dilatation of distal bowel -> megacolon.


What % of upper GI bleeding is thought to be caused by Malory-Weiss tears. Give a brief description of this phenomenon.

10% of all upper GI bleeds.

Usually caused by violent or repetitive wretching and/or vomitting. Results in longtitudinal tears of the GI mucosa at the gastro-oesophageal sphincter. Usually range from a few mm to several cm in length. Heal rapidly and very rarely require intervention.


What two types of Ca result in the majority of oesophageal Ca?

  1. Adenocarcinoma (often preluded by Barrett's oesophagitis, and
  2. Squamous cell carcinoma.


List the factors that protect the gastric mucosa from the extremely high acidity (pH=1) in the stomach.

Discuss mechanisms that may interfere with these protective mechanisms.

  1. Mucin produced by foveolar cells in the cardia and antrum form a protective barrier;
  2. Bicarb secretion into mucin by epithelial cells - neutral pH;
  3. Rich vascular supply delivers  nutrients and washes away diffused acid;
  4. Production of prostaglandins by epithelial cells are protective

Injury can be caused by:

  • Reduced mucin production - age-related;
  • NSAIDs - reduce prostaglandins and bicarb prod'n
  • H.pylori - interruption of bicarb transporters
  • Toxins - direct injury to epithelial cells (poisons, NSAIDs, tobacco smoke, ETOH, rad'n, chemo)
  • Mitotic inhibitors - eg colchicine, chemo agents -> red'd mucosal turnover (normally 100% turnover every 2-6days)
  • Reduced O2 delivery - eg high altitude


List the four types of cells commonly found in the gastric pits and their functions.

  1. Foveolar cells - produce mucin 
    1. Surface mucus cells: produce mucin with high pH due to bicarb production
    2. Mucus neck cells: produce mucin with lower pH
  2. Chief cells: Produce pepsinogen and gastric lipase
  3. Parietal Cells: Produce intrinsic factor and HCl
  4. G-Cells: Secrete gastrin into the blood


List the three complications of gastric ulcers.

  1. Bleeding:
  • Occurs in 15-20% of patients with PUD
  • Most common complication, accounts for 25% of PUD deaths
  1. Perforation:
  • Occurs in up to 5% of patients with PUD
  • Accounts for 2/3 of PUD deaths
  1. Obstruction:

  • Occurs in up to 5% of patients with PUD 

  • Secondary to oedema and scarring
  • Usually in the pylorus and duodenum


Describe the components of the foregut. Which artery supplies this region?

  • Abdominal oesophagus
  • Stomach
  • Duodenum D1 and D2 until just distal to the major duodenal papilla
  • Liver 
  • Gall bladder
  • Pancreas
  • Spleen

Arterial supply of foregut is via the Celiac Trunk.


What is inflammatory bowel disease?

Inflammatory Bowel Disease is a chronic inflammatory disease that results from inappropriate mucosal immune activation.

It is comprised of:

  • Crohn Disease, and
  • Ulcerative Colitis.


How do Crohn Disease and Ulcerative Colitis differ?

  • CD: Involves ileum and colon - skip lesions
  • UC: Colon only - continuous


  • CD: Transmural
  • UC: Mucosa only


  • CD: Thickened bowel wall
  • UC: Thinned bowel wall - inc'g pseudopolyps




What is the pathogenesis of IBD?

Uncertain. Thought to be a combination of:

  • defects in interaction btw host defences and bacterial flora,
  • epithelial dysfunction, and 
  • aberrant mucosal immune responses.


What is the mainstay of treatment for IBD?

Immunosupression +/- surgery in UC > CD.


List some of the extra-GI manifestations of IBD.

  • Uveitis
  • migratory polyarthritis
  • sacrolilitis
  • ankylosing spondilitis
  • pericholangitis and sclerosing cholangitis (UC>CD)
  • Inc'd risk of colonic Ca.


Discuss diverticulitis.

  • Disease of older patients - 50% by age 60yrs
  • Can remain asymptomatic
  • Increased intraluminal pressures lead to outpouchings at sites where vessels and nerves pass through the intestinal muscle wall -> diverticulum.
  • Low fibre diets -> constipation -> inc'd risk
  • Can lead to diverticulitis and perforation - diverticular abcess and/or peritonitis


List the common causes of ischaemic bowel disease. 

Can be acute or chronic.

Can result in transmural ischaemia or partial thickness (mucosal/submucosal)

Common predisposing conditions include:

  • Severe atherosclerosis
  • Aortic aneurysm
  • Hypercoaguable states
  • Embolisation of cardiac vegetations or aortic atheromas
  • OCP use
  • Vasculitides - Wegner granulomatosis, Henloch-Scholein purpura, polyarteritis nodosum
  • Hypoperfusion - Cardiac failure, shock, dehydration, vasoconstrictive drugs.



List two common chronic malabsorptive conditions. Give a brief explanation of how these conditions result in malabsorption.

  • Celiac disease - Chronic autoimmune disorder caused by an abnormal reaction of the mucosal cells to gliadin (gluten protein) which induces an inflammatory reaction that results in villous atrophy -> malabsorption within the small bowel (carbs, fats, fat-soluble minerals and vitamins (iron, B12, folate, Vit D, Calcium) -> wt loss, anaemia, osteopaenia
  • CF - Chloride ion secretion problems -> bicarb, sodium and water secretion -> blockage of ducts -> autodigestion of the pancreas -> pancreatic enzyme insufficiency


What are the five common responses to hepatocellular injury?

  1. Hepatocyte degeneration and intracellular accumulations
  2. Hepatocyte necrosis and apoptosis
  3. Inflammation
  4. Regeneration
  5. Fibrosis


What are the common syndromes that result from hepatocellular injury?

  • Hepatic failure
  • Cirrhosis
  • Portal hypertension
  • Bilirubin metabolism problems -> jaundice and cholestasis


Discuss hepatic failure.

  • Can be acute or chronic
  • End-stage of many hepatic disease
  • 80-90% of liver function must be lost before hapatic failure results
  • Results in failure of normal hepatic functions:
    • jaundice
    • coagulopathy due decreased clotting factors
    • hypoalbuminaemia -> peripheral oedema
    • hyperammonaemia -> encephalopathy 
    • fetor hepaticus
    • impaired oestrogen metabolism -> hyperoestrogenaemia
    • renal failure (hepatorenal syndrome)
    • hepatopulmonary syndrome


List the common causes of acute liver failure.

  • Paracetamol toxicity (50%)
  • Other drugs and toxins (eg halothane, rifampicin, isoniazid, MAOIs) (14%)
  • Hepatitis A virus (4%)
  • Hepatitis B virus (8%)
  • Autoimmune disease (12%)
  • Unknown (15%)



Discuss cirrhosis.

  • Represents liver scarring -> normal hepatocytes are replaced by fibrous tissue
  • Types I & III collagen are found in the cirrhotic liver
  • Leads to nodules of normal hepatocytes surrounded by fibrous tissue -> compromised blood flow, inability of remaining hepatocytes to deliver substances into blood, obliteration of biliary channels -> jaundice.
  • Remain asymptomatic until late stages
  • Results in:
    • anorexia, wt loss, weakness
    • signs and symptoms of liver failure
    • portal hypertension
    • progressive liver failure
    • development of hepatic Ca.


List the five most common causes of cirrhosis.

  • alcoholic liver disease
  • viral hepatitis
  • non-alcoholic fatty liver disease
  • biliary disease
  • iron overload


Discuss the common causes of portal hypertension.

  • Pre-hepatic causes:
    • obstructive thrombosis
    • portal vein stenosis
    • massive splenomegaly
  • Intra-hepatic causes:
    • cirrhosis
    • sarcoid
    • schistosomiasis
    • massive fatty change
  • Post-hepatic causes:
    • severe right heart failure
    • constrictive pericarditis
    • hepatic vein outflow obstruction


List the 3 stages of alcoholic liver disease.

  1. Hepatic steatosis (fatty liver disease)
  2. Alcoholic hepatitis
  3. Cirrhosis


What factors increase the risk of developing ETOH liver disease?

  • ETOH intake
  • Gender F > M
  • Ethnicity
  • Genetic factors
  • Co-morbid conditions - Fe overload, viral hepatitis


What are the common complications of portal hypertension?

  • Oesophageal varices
  • Ascites
  • Spontaneous bacterial peritonitis
  • Splenomegaly
  • Hepatorenal syndrome
  • Hepatic encephalopathy


What is hepatic encephalopathy?

Altered LOC as the result of a build-up of toxic metabolites (eg ammonia) normally metabolised by the liver, in the setting of hepatic failure.


List the common modes of transmission of Hep C Virus  (HCV).