Alimentary Pathology

Question 1

Describe Meckel’s Diverticulum

Answer 1

A small bulge in the small intestine present at birth due to the remnant of the embryonic vitelline duct persisting. Often asymptomatic but symptoms include bleeding, obstruction, inflammation or perforation.

Question 2

Outline the consequences and the types of obstruction that may occur within the GI tract

Answer 2

Consequences: Interrupted peristaltic movements, abdominal distension, pain Types: Volvulus (twisting), fistula (joining between adjacent structures), intussception (‘folding’ back of the wall), hernation

Question 3

Outline chronic inflammation

Answer 3

Chronic inflammation is descriptive of the simultaneous occurrence of inflammation and repair at the same time within a tissue. Macrophages, plasma cells, eosinophils and leukocytes are associated with chronic inflammation Causes include bacteria which cannot be cleared, viral infection, exposure to toxins and autoimmune diseases

Question 4

Which features do Crohn’s disease and Ulcerative Colitis are common?

Answer 4

• Both are due to immune recognition of the bodies own flora
• Both are chronic relapsing inflammatory diseases
• Both have systemic effects
• Both are more common within the Western population

Question 5

Describe the features of Crohn’s disease

Answer 5

A chronic granulomatous inflammatory condition. Crohn’s disease sees damage to the whole wall of the GI tract, resulting in the formation of cobblestone lesions.

Skip lesions may occur, as portions of the GI tract remain unaffected. Crohn’s may affect any part of the GI tract.

The GI wall becomes scarred and fibrosed, leading to sclerosis and thickening of the wall. If the wall is eroded then the intestine may adhere to adjacent structures. forming fistulas.

Associated with certain HLA allelles

Symptoms: Colicy pain, diarrhoea

Question 6

Describe the features of Ulcerative Colitis

Answer 6

A chronic inflammatory condition which affects the mucosal layer of the GI tract. Pseuodpolyps form and the GI wall undergoes thinning, leading to dilation. The glands of the GI tract are damaged, becoming short and branched (rather than the long, straight glands that are normally observed).

The condition affects the colon, with spread to the rectum and anus possible.

Symptoms: Bloody watery diarrhoea,

Question 7

Give examples of causes of malabsorption (4)

Answer 7

1. Insufficient bile production 2. Insufficient pancreatic enzymes (may be related to secretion, e.g. CF) 3. Decreased surface area 4. Decreased brush border enzymes (e.g. due to destruction)

Question 8

Describe the features of Coeliac disease

Answer 8

Coeliac disease is resultant of an inflammatory response (T cell) triggered by dietary gluten, once broken down into gliadin. Relation to the HLA haplotype.

Most severe in the proximal small intestine, as this is where gluten exposure is maximum.

Inflammation in the gut causes blunting of the villi (villous atrophy) and gland hyperplasia.

Infiltration of leukocytes is increased within the mucosa and lamina propria.

Symptoms: Abdominal distension, steatorrhoea, faltering growth, abdominal pain

Question 9

Investigations for Coeliac disease

Answer 9

Anti-tTG: Produced from the breakdown of gluten. Antibodies directed against the molecule. Anti-EMA: Autoantibodies directed against the endomysium of muscle (contains a form of tTG) Serology of IgA (mucosal antibody)

Question 10

Describe the features of Cystic Fibrosis

Answer 10

Cystic fibrosis is resultant of a defect in the CFTR gene, most commonly delta508, which leads to an inability to transport chloride ions using the transporter.

This has an effect on osmotic potential/movement.

In the respiratory and pancreatic epithelium this means that active transport of chloride out of the cell cannot occur. Transport of sodium into the cell increases, water follows, leading to mucus becoming very viscous.

Consequences: Decreased respiratory clearance, blocking of pancreatic glands/ducts leading to malabsorption, blockage of hepatic canaliculi (may lead to fibrosis)

Question 11

Describe the features of Diverticulosis

Answer 11

Diverticulosis sees out-pouching of the wall of the intestine, which may become inflamed or infected.

Possible due to the discontinuous longitudinal muscle of the large intestine (taenia coli) and circular bands.

Risk factors: Increasing age, low fibre diet, poor bowel habit

Question 12

Name the 3 subclasses of jaundice

Answer 12

Pre-hepatic: Haemolytic Intra-hepatic: Hepatitis, NASH Post-hepatic: Obstruction of the biliary tree (cholestasis), cholelithiasis

Question 13

Describe the metabolism of bilirubin

Answer 13

Bilirubin is breakdown product of haem (RBCs) Bilirubin in it’s pre-hepatic form is unconjugated and therefore insoluble. Within the liver bilirubin undergoes conjugation, becoming soluble. Urobilogen results. This is secreted into the bile. Within the GI tract (as bile) urobilogen undergos further reactions to sterobilin. Excreted in the faeces - provides pigment. Urobilogen may be reabsorbed into the blood, into the kidneys and excreted in urine as urobilin. This also provides pigment to the urine.

Question 14

Features of jaundice subclasses

Answer 14

Pre-hepatic: Increased levels of unconjugated bilirubin observed. Intra-hepatic: Pale stools, dark urine Post-hepatic: Pale stools, dark urine and itching,

Question 15

Jaundice: Definition

Answer 15

Jaundice is yellowing of the skin, particularly observed within the sclera of the eyes. Jaundice is resultant of increased build-up of bilirubin within the skin

Question 16

Post-hepatic/Obstructive jaundice: Diagnosis, investigations and management

Answer 16

Diagnosis: Yellowing, anorexia, pruritus, stool and urine colour, check for Murphy’s sign, check for fever (cholecystitis GB)

Investigations: Urine (conjugated bilirubin), blood test (bilirubin levels, iron levels), LFTs (synthetic function, ALT/AST); X-ray; ultrasonography; CT; MCRP; MRI; ERCP

Management: Removal of gallstones

Question 17

Courvoisier sign

Answer 17

In the presence of an enlarged palpable gall bladder, which is NON-TENDER, and mild jaundice the cause is unlikely to be gallstones

Question 18

Describe the pathogenesis of liver cirrhosis

Answer 18

Commonly a progression of hepatitis or steatosis. Damage to the liver leads to hepatocyte necrosis and subsequent release of cellular contents and ROS. This activates hepatic Kupffer cells, which secrete pro-inflammatory cytokines. Stellate cells are also activated. They secrete collagen allowing fibrotic cross-bridges to form between the portal tracts (fibrous septa) Bulging regenerative nodules surrounded by fibrotic tissue are seen.

Question 19

AFLD: Describe the associated metabolic changes

Answer 19

Hypoglycaemia: Decreased gluconeogenesis and glycogenolysis Acidosis: Due to accumulation of pyruvate and hence conversion to lactate, generating H of Liver.. Steatosis: Decreased lipolysis and increased synthesis of fat

Question 20

Cirrhosis: Outline the consequences of cirrhosis

Answer 20

Reduced blood flow in the liver

Hepatic encephalopathy (as toxic metabolites accumulate) Reduced hepatic synthetic ability

Reduced synthesis of bile

Portal hypertension: As blood flow through the liver is obstructed this causes an accumulation of blood, raising pressure within the system.

Question 21

Colorectal cancer: Describe the pathogenesis of colorectal cancer

Answer 21

Normal epithelium → Hyperplastic epithelium → Adenoma → Carcinoma

Aberrant APC splicing, oncogenes and tumour suppressor genes are all implicated in the progression of colorectal cancer

Hyperplastic epithelium: Such as the growth of polyps (abnormal cell growth projecting from a mucous membrane)

Most commonly seen in the caecum and sigmoid colon

Question 22

Colorectal cancer: List risk factors for the development of colorectal cancer

Answer 22

Male > 50 years of age APC/FAP mutation Diet high in processed foods and low in fibre IBD Obesity Lynch syndrome (genetic predisposition to cancers)

Question 23

Describe the normal structure of the gut mucosa

Answer 23

Question 24

Outline the progression of hepatitis/steatosis in the liver

Answer 24

Question 25

Describe the innervation of the abdominal wall

Answer 25

• Ventral rami of 6th to 11th intercostal nerves
• Ilioinguinal
• Iliohypogastric

Question 26

Gastric ulcers: Describe the appearance of benign gastric ulcers and common causes

Answer 26

Appearance: Open sore with defined margins (chronic inflammation)

Common causes: H. pylori infection, NSAID use

May also occur in the duodenum - duodenal ulcers

Outcomes: Bleeding, anaemia, GORD

Question 27

Gastric mucosa: Describe the structure of the mucosa present in the stomach, include cell types

Answer 27

• Gastric mucosa forms villi and gastric glands/crypts of Lieberhans
• The gastric glands are formed from various cell types:
  
  • Mucous cells
  • Parietal cells
  • Chied cells
  • G cells
  • Enteroendocrine cells

Question 28

Inguinal canal: Describe the formation of a direct inguinal hernia

Answer 28

• Abdominal contents protrude through the wall of the inguinal canal
• The contents emerge at the superficial ring of the inguinal canal

REMEMBER: The inguinal canal at the midpoint of the inguinal ligament (from the ASIS to pubic tubercle)

Question 29

Inguinal canal: Describe the formation of an indirect inguinal hernia

Answer 29

• Abdominal contents enter the deep ring of the inguinal canal
• The contents then emerge at the superficial ring of the inguinal canal
• Protrusion is more likely to occur due to this path of herniation being less ‘resistant’

Question 30

Digestive defects: Outline the main causes of digestive defects

Answer 30

• Schwann-man Diamond syndrome: Failure to produce pancreatic digestive enzymes
• Cystic fibrosis: Can cause blockage in the ducts of the pancreas and liver, preventing the release of digestive enzymes and bile respectively
  
  • Can cause diabetes
• Loss of bile synthesis
• Defective enterokinase (no activation of trypsin)

Question 31

Outline the possible mechanisms of diarrhoea

Answer 31

• Inflammatory: Inflammation following infection
• Non-inflammatory
  
  • Secretory: Caused by a_bnormal transport of ions_ across the mucosa of the GI symstem
  • Osmotic: The presence of poorly absorbed solute in the intestine leads to the movement of water into the lumen/osmotic movement

Question 32

Describe the cellular morphology seen in different types of anaemia

Answer 32

Question 33

Outline the clinical significance the rectouterine pouch and the vesicouterine

Answer 33

Rectouterine pouch: Between the rectum and the uterus

Analagous to the rectovesical pouch in males

• The lowest and most dependent part of the abdominal cavity
• Leads to the accumulation of fluids in this area in supine female patients
• Drained in end-stage renal failure

Vesicouterine pouch: Between the uterus and the bladder

Question 34

Ascites: Common causes of ascites

Answer 34

• Portal hypertension
• May also be caused by: Infection, heart failure, malnutrition, malignancies of the GI tract.