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*Medicine: Cellular Pathology > Gastrointestinal pathology (1) > Flashcards

Gastrointestinal pathology (1) Flashcards

1
Q

What is the generic histological structure of the GI tract?

A
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2
Q

The structure of the GI tract is relatively constant throughout. Which of the 5 histological GI layers varies throughout the GI tract?

A

Mucosa

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3
Q

Hence, describe the mucosal structure in the following:

  • Oesophagus
  • Stomach
  • Small Intestine
  • Colon + rectum
A
  • oesophagus: white stratified squamous (a transit tube)
  • stomach: red-brown thick glandular (storage + digestion)
  • small intestine: glandular w/ villi (nutrient absorption)
  • colon + rectum: glandular w/ crypts (water absorption)
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4
Q

What is gastro-oeseophageal reflux?

A
  • there is regurgitation of acidic gastric contents into lower oesophagus
  • acid injures the squamous epithelium lining the oesophagus
  • results in inflammation (reflux oesophagitis)
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5
Q

What are the risk factors for developing GORD?

A
  • obesity + pregnancy (inc intra-abdo pressure)
  • smoking, alcohol, coffee consumption (lowers oesophageal sphincter tone)
  • hiatus hernia
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6
Q

What is a hiatus hernia?

A
  • protrusion (or herniation) of the upper part of stomach
  • into the thoracic cavity
  • thought to be due to combo of diaphragmatic weakening + inc intra-abdo pressure
  • the major clinical effect = weakening of lower oesophageal sphincter mechanism
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7
Q

What is the presentation + associated complications of GORD?

A
  • Heartburn (major feature) relieved by antacids
  • Regurgitation -> waterbrash
  • Belching
  • Oeseophagitis
  • Stricture (progressive dysphagia)
  • Bleeding (haematemesis, melaena)
  • Barrett’s oesophagus
  • Nocturnal asthma + chronic cough
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8
Q

A complication of GORD is Barrett’s oeseophagus (10%). What is Barrett’s oesophagus?

A
  • when normal oeseophageal squamous epithelium replaced
  • by metaplastic columnar mucosa
  • form segment of ‘columnar-lined oeseophagus’
  • an adaptive response to prolonged injury caused by GORD
  • asymptomatic - most cases identified when pts undergo OGD (for GORD/dyspepsia)
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9
Q

What % of those with Barrett’s Oesophagus progress to oeseophageal cancer?

A
  • 0.1-0.4%
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10
Q

What does metaplasia do to the squamous mucosa lining in the oesophagus?

A

Metaplasia in Barrett’s Oesophagus:

  • Normal squamous mucosa replaced with glandular (columnar) mucosa
  • Due to reflux of gastric acid (as the insult)
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11
Q

What may the metaplastic columnar epithelium progress to next?

A
  • Dysplasia (occurs in 2% of those with Barrett’s)
  • And then into an invasive adenocarcinoma
  • This is known as the metaplasia-dysplasia-carcinoma sequence
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12
Q

Why and how is dysplasia identified and managed in patients?

A
  • Bc development of oesophageal adenocarcinoma (malignant) is preceded by a phase of dysplasia (pre-malignant)
  • some gastroenterologists perform surveillance endoscopy w/ biopsies at 3-5yr intervals to look for dysplasia
  • if dysplasia identified, intervention (eg radiofrequency ablation or endoscopic mucosal resection) is advised
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13
Q

What is characteristic of the adenocarcinoma that the dysplasia doesn’t demonstrate?

A

Invasion through the basement membrane

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14
Q

Who is oesophageal cancer common in?

A
  • 50-70yr age group
  • M > F
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15
Q

How does oesophageal cancer present?

A
  • Progressive dysphagia (of solids first then liquids too)
  • Weight loss
  • Anorexia
  • Lymphadenopathy
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16
Q

What are the key investigations?

A
  • endoscopy
  • biopsy
    • type of cancer
    • grade
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17
Q

What is the most common type of oesophageal cancer in the UK?

A
  • adenocarcinoma (70% of all new OCa diagnoses)
  • marked rise in incidence in western world in last 30ys
  • usually arises from Barrett’s mucosa in lower oesophagus
  • remember that progression from Barrett’s -> cancer is not inevitable
  • in fact, risk of dying from oesophageal adenocarcinoma in a pt with Barrett’s is 2% over 10 years (less than the risk of dying from ischaemic heart disease!)
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18
Q

What is the second most common type of oesophageal cancer in the UK?

A
  • squamous cell carcinoma
  • most common type in other parts of world eg. china, japan
  • oesophageal squamous cell carcinoma arises from native oesophageal squamous epithelium
  • important risk factors for its development = smoking + alcohol
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19
Q

How is oesophageal cancer staged?

A
  • TNM system
  • performed using range of techniques
    • eg. EUS, chest/abdo CT, laparoscopy
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20
Q

What is discussed at an MDT meeting for oesophageal cancer?

A
  • decide on most appropriate treatment
  • curative intent (surgery with/without neoadjuvant therapy)
  • palliative intent (eg. dilatation, stenting, radiotherapy etc)
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21
Q

What is the prognosis for oesophageal cancer?

A
  • 5-10% survival at 5 years
  • this is mainly bc tumor is usually at high stage on presentation
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22
Q

What is gastritis?

A
  • strictly speaking, refers to inflammation in stomach
  • however, in clinical practice it is often used to describe any redness of the gastric mucosa seen at endoscopy
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23
Q

What are 2 important causes of gastritis?

A
  1. NSAIDs
  2. Helicobacter Pylori infection
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24
Q

What is H. Pylori and how does it survive?

A
  • gram negative bacteria that colonises stomach
  • spread by oral-oral or faecal-oral transmission
  • it lives in the thick mucus layer on mucosal surface
  • H. pylori synthesises urease, which catalyses conversion of urea to ammonia. The ammonia neutralises the gastric acid and thus improves survival of the bacteria
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25
Q

Gastric H. Pylori is associated with a range of consequences, such as?

A
  • > 80% of pts have an asymptomatic mild chronic gastritis
  • a minority of pts develop symptomatic gastritis
  • a minority of pts develop a peptic ulcer
  • a small minority of pts develop gastric carcinoma
  • a v small minority of pts develop gastric lymphoma
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26
Q

What is a peptic ulcer?

A
  • breach in mucosa of the lower oesophagus, stomach or duodenum, extends through full thickness of mucosa and in addition may extend into the submucosa or deeper layers of wall
  • fails to heal over a reasonable period of time
  • most comonly located in the gastric antrum or proximal duodenum
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27
Q

What is the commonest cause of gastric and duodenal peptic ulcers?

A
  • H pylori gastritis
  • NSAIDs
  • also: alcohol, smoking + stress
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28
Q

What is a Curling (stress) ulcer?

A
  • seen in pts with massive trauma, extensive burns, sepsis, raised intracranial pressure or shock
  • thought to arise as a consequence of mucosal ischaemia leading to inc susceptibility to acid pepsin injury
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29
Q

What is the commonest cause of oesophageal peptic ulcers?

A

Gastro-oesophageal reflux

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30
Q

Are peptic ulcers due to cancer?

A

No, they are a good example of chronic inflammation

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31
Q

How are peptic ulcers a good example of chronic inflammation?

A

there is simultaneous:

  • persistent tissue injury + destruction at surface
  • on-going inflammatory response to limit damage
    • the main inflammatory cells are macrophages, lymphocytes and plasma cells
  • attempts to organise and heal by fibrosis (scarring)
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32
Q

What is the pathogenesis of peptic ulceration?

A
  • mucosal surfaces normally coming into contact w/ gastric acid + pepsin have evolved a # of defence mechanisms
    • surface-adherent mucus/bicarb layer, epithelial cell defences + mucosal blood flow
      ​
  • peptic ulcers can occur by weakening of these defence mechs or by increased acid attack
  • surface mucus is significantly disrupted by H pylori
  • epithelial cell defences are undermined by the cytotoxic effects of H pylori and NSAIDs
  • mucosal blood flow alterations probs more important in acute ulcers occurring in clinical states of shock
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33
Q

What is Zollinger-Ellison syndrome + how does it lead to peptic ulceration?

A
  • tumours from pancreas, stomach or duodenum secrete large amounts of gastrin (gastrinomas)
  • cause excess gastric acid secretion
  • therefore increased acid attack -> weakened defence system against peptic ulcer
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34
Q

What are complications of peptic ulcers?

A
  • bleeding
  • perforation
  • stricture formation
  • malignant change
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35
Q

How do acute bleeds of peptic ulcers present?

A
  • when an ulcer erodes wall of a large vessel, tend to be large
  • presents with melaena or haematemesis
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36
Q

How does chronic bleeding from peptic ulcers present?

A
  • typically multiple smaller bleeds (compared to acute)
  • over a long period of time
  • may present as anaemia
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37
Q

What is the term used to describe when a peptic ulcer erodes through all the layers of the wall? How does this present?

A
  • perforation
  • present as peritonitis
38
Q

How might stricture formation due to peptic ulcer present?

A
  • due to healing of the ulcer by fibrosis
  • may present as obstruction
39
Q

Is the development of carcinoma a common complication of peptic ulcers?

A
  • No, it’s rare
  • in fact, it’s now believed that reports of malignant transformation in peptic ulcers probably represents cases in which a lesion thought to be a chronic peptic ulcer was actually an ulcerated carcinoma from start
  • ulcerated gastric carcinomas typically have a rolled edge
40
Q

What investigation should be done from any suspected peptic ulcer in the oesophagus or stomach to rule out that it isn’t actually an ulcerated cancer?

A

Biopsy

NB. Dudoenal cancer is v rare and so chance of duodenal cancer masquerading as a peptic ulcer is remote. Hence duodenal ulcers do not need to be biopsied to exclude malignancy unless there are worrying endoscopic features.

41
Q

Who is gastric cancer common in? Has the incidence changed?

A
  • peak incidence in over 50yr age group
  • M > F
  • incidence has fallen in west over last 50yrs
  • reduction due to falling prevalence of H pylori infection and an improved diet
42
Q

What are important risk factors for developing gastric cancer?

A
  • H Pylori infection (but remember, most ppl w H Pylori infection will not develop cancer)
  • cigarette smoking
  • alcohol
  • diet: food w/ nitrates/nitrite components; salt-based preservatives
  • autoimmune gastritis
43
Q

How might gastric cancer present?

A
  • history of new-onset dyspepsia (esp in a pt >55y)
  • unintended weight loss
  • progressive dysphagia
  • vomiting
  • Virchow’s node palpable (left supraclavicular fossa) - Troiser’s sign
44
Q

What kind of cancer are gastric cancers?

A
  • adenocarcinomas
  • arising from glandular mucosa
45
Q

What are the 2 main types of gastric adenocarcinoma and how do they differ?

A
  • intestinal-type adenocarcinomas - show gland formation, lined by mucus-secreting cells. Better prognosis than diffuse-type (but still poor 5 year survival). Tend to occur in older individuals.
  • diffuse-type adenocarcinomas - consist of ‘signet-ring’ cells, with a diffuse pattern of infiltration. Very aggressive -> v bad prognosis. Tends to occur in a younger age group.
46
Q

They key investigation for gastric cancer is endoscopy and biopsy. What important info does biopsy give us?

A
  • type of cancer (usually squamous cell carcinoma or adenocarcinoma)
  • the grade - well, moderately or poorly differentiated
47
Q

How is gastric cancer staged?

A
  • TNM system
  • performed using a range of techniques
  • eg. chest/abdo CT, staging laproscopy
48
Q

All pts with gastric cancer are discussed at the MDT meeting to decide on most appropriate treatment: curative or palliative. What is the prognosis of gastric cancer?

A
  • very poor prognosis
  • around 5% survival at 5 years
  • mainly bc tumour is usually at high stage on presentation
49
Q

How much of the adult Western population develop gallstones?

A
  • 10-15%
  • Each year approx 2-4% of ppl with gallstones develop symptoms, in other words most people are asymptomatic
50
Q

What is the pathogenesis of gall stones?

A

Normally cholesterol is solubilised in bile as a micelle with bile salts.

An imbalance between the proportions of cholesterol and bile salts lead to precipitation of the excess component as gallstones.

51
Q

What are the 3 types of gallstones?

A
  • cholesterol stones (20%) - large, yellow
  • billirubinate stones (5%) - small, pigmented (dark)
  • mixed stones (75%) - Ca salts, bile pigment + cholesterol
52
Q

What are the risk factors for cholesterol gallstone formation?

A
  • female sex
  • obesity
  • middle-age
  • family history

all are associated w inc levels of cholesterol -> results in imbalance between cholesterol + bile salts and the precipitation of gallstones

53
Q

What link does Crohn’s disease have to gallstones?

A
  • Crohn’s predisposes to development of gallstones
  • Due to malabsorption of bile salts from terminal ileum
  • Affected individual becomes depleted in bile salts
  • They do not have enough bile to maintain the cholesterol dissolved in bile
  • Thus cholesterol stones form
54
Q

What can cause bilirubinate gallstones?

A
  • Haemolytic anaemias
  • Cause inc bilirubin production (bc of XS breakdown of Hb)
  • Results in an imbalance between cholesterol + bile salts
  • Thus, the bile salts precipitate as gallstone
55
Q

What investigations can be done for gallstones?

A
  • Ultrasound of gallbladder -> identify 90% of gallstones
  • Liver function tests to assess liver fxn
56
Q

What ducts meet to form the common bile duct?

A
  • Cystic duct from gallbladder
  • Common hepatic duct (from R + R hepatic ducts)
  • Come together to form common bile duct (outside the liver)
57
Q

Remember, most patients with gallstones are asymptomatic. How might patients with symptomatic gallstones present?

A
  • Biliary colic or cholecystitis (>90% of symptomatic presentations)
  • Jaundice +/- ascending cholangitis
  • Acute pancreatitis
  • Gallstone ‘ileus’
58
Q

How does a biliary colic come about and how does this present?

A
  • if a gallstone impacts in + obstructs the cystic duct
  • the gallbladder will contract against the acutely obstructed duct
  • resulting in symptoms of biliary colic:
    • upper abdo/RUQ pain, may radiate to back/tip of scapula, often nausea + vomiting
59
Q

How does acute cholecystitis develop from a gallstone?

A
  • if the impacted stone occludes cystic duct for a prolonged period of time
  • it will rub + damage the mucosal lining
  • thereby inciting an acute inflammatory response in gallbladder wall
  • there is development of acute cholecystitis
  • presence of fever indicates acute cholecystitis (or cholangitis)
60
Q

What is acute acalculous cholecystitis?

A
  • acute cholecystitis without gallstones
  • thought to result from ischaemia
  • the cystic artery is an end artery w/ no collateral circulation
  • it occurs in pts who are hospitalised for conditions unrelated to gallbladder eg. hypotension + multiorgan failure; major trauma/burns; infections
  • clinical symptoms tend to be insidious since they are obscured by underlying condition
  • a high % of pts have no symptoms referable to gallbladder; diagnosis therefore rests on a high index of suspicion
  • as a result of either delay in dx or disease itself, incidence of gangrene + perforation is much higher in acalculous cholecystitis than cholecystitis due to gallstones
61
Q

What is chronic cholecystitis?

A
  • repeated episodes of biliary colic + acute cholecystitis
  • results in chronic inflammation w/ healing by fibrosis
  • as a consequence, gallbladder wall becomes thickened + the gallbladder shrinks in size
62
Q

How do gallstones cause jaundice?

A
  • if a gallstone impacts + obstructs the common bile duct (choledocholithasis), it will cause obstructive jaundice
  • the jaundice develops bc bile is unable to drain into the duodenum for excretion
63
Q

A serious complication of a gallstone obstructing the common bile duct is the development of ascending cholangitis. What is this?

A
  • inflammation of common bile duct
  • the biliary obstruction causes stasis
  • predisposes to superimposed infection: gut bacteria (usually gram negative eg. E coli, Klebsiella) gain entry to biliary tree via ampulla of Vater
64
Q

How does ascending chlangitis typically present clinically?

A
  • Charcot’s triad
  • jaundice, fever (usually w rigors) + RUQ pain
65
Q

What happens if ascending cholangitis is left untreated?

A
  • infection may ascend up to the liver
  • causing abscesses
  • and/or cause sepsis
  • serious condition if left untreated has a high mortality
66
Q

Gallstones are the commonest cause of acute pancreatitis. How do gallstones cause acute pancreatitis?

A
  • if gallstone passes down common bile duct
  • obstructs Ampulla of Vater
  • results in pancreatitis
  • there is reflux of pancreatic secretions back up the pancreatic duct -> pancreatic autodigestion -> pancreatitis
67
Q

What is the other major cause of pancreatitis apart from gallstones?

A

alcohol

68
Q

What is gallstone ‘ileus’?

A
  • When a large gallstone causes small bowel obstruction
  • Stone erodes through gallbladder into duodenum; then obstructs terminal ileum
  • Gallstone enters the small bowel via a fistula, which forms between the inflamed wall of GB and a loop of small bowel
69
Q

Why is gallstone ‘ileus’ a misnomer?

A
  • Ileus is characterised by cessation of normal peristaltic movements of bowel, typically a rxn of the bowel to any form of irritation around it (eg. post-op, peritonitis)
  • If a gallstone obstructs the small bowel, the small bowel proximal to the obstruction will attempt to overcome the blocokage by vigorous peristalsis

Hence, the term gallstone ‘ileus’ is incorrect

70
Q

What is the clinical presentation of gallstone ileus?

A

Cardinal features of bowel obstruction

  • colicky abdo pain
  • vomiting
  • abdominal distension
  • absolute constipation
71
Q

What does Courvoiser’s Law state and why?

A

“In a jaundiced patient, the presence of a palpable gallbladder means that the jaundice is unlikely to be due to gallstones impacted in the biliary system”

  • bc a pt w/ jaundice due to gallstone in the common bile duct is likely to have a fibrotic shrunken gallbladder bc of repeated episodes of biliary colic + acute cholecystitis - as a consequence, the gallbladder is impalpable
  • a patient w/ jaundice due to another cause may have a palpable gallbladder
72
Q

What is another cause of a palpable gallbladder, unrelated to gallstones?

A

Often (but not necessarily) cancer of the head of the pancreas

73
Q

What are the two broad functions of the pancreas?

A
  • Exocrine - secreting digestive enzymes into the pancreatic duct system
  • Endocrine - secreting hormones such as insulin and glucagon directly into the blood
74
Q

What is the most common type of pancreatic cancer?

A
  • Adenocarcinoma
  • Arises from glandular duct cells that line ducts of exocrine system
75
Q

Who is pancreatic adenocarcinoma common in?

A
  • Elderly males
  • Very little is known about underlying cause
  • Smoking is only well recognised risk factor
76
Q

Most pancreatic adenocarcinomas involve the head of the pancreas. What do they present with?

A
  • Obstructive jaundice
    • tumour compresses common bile duct as it passes through the head of pancreas so that bile is unable to drain into duodenum
  • other features: weight loss, mid-epigastric pain (often radiating to back)
77
Q

What is the treatment for majority of pancreatic carcinoma patients?

A
  • 80% of pts with pancreatic carcinoma have advanced disease (high stage) at time of dx
  • treatment is palliative
  • palliative treatment options:
    • chemotherapy
    • stenting the common bile duct to relieve jaundice
    • optimising symptom control
78
Q

A minority of pancreatic carcinoma patients (20%) are suitable for curative surgery - Why are they suitable? What is the procedure called?

A
  • bc tumour appears to be confined to pancreas and lymph nodes are not involved
  • Whipple’s procedure
79
Q

What happens in a Whipple’s procedure?

A

The distal stomach, gallbladder, common bile duct, head of pancreas, duodenum, proximal jejunum and regional lymph nodes are resected.

Reconstruction restores intestinal fxn by re-establishing flow of pancreatic juices, bile and food along GI tract.

80
Q

What is the 5 year survival following a) curative surgery (Whipple’s) and b) overall survival for pancreatic cancer?

A

A) Whipple’s - 20-40%

B) 5% (incl majority of pts who have advanced disease)

81
Q

How common is Coeliac disease?

A

Affects ~ 1% of UK population

82
Q

What is Coeliac disease?

A
  • intolerance to gluten
  • in particular, gliadin, the alcohol-free fraction of gluten, is the disease-producing component
  • gluten is found in wheat, barley and rye
83
Q

What is the brief pathogenesis of coeliac disease?

A
  • not fully understood
  • thought that gliadin triggers inappropriate activation
  • of intestinal T cells
  • in genetically susceptible individuals (ppl w/ HLA-DQ2 and HLA-DQ8 haplotypes)
  • resulting in damage to epithelial cells
84
Q

Now explain in more detail what happens in patients with coeliac when gluten is digested in comparison to a healthy individual?

A
  • gluten digested by luminal and brush-border enzymes in small intestine
  • into aino acids + peptides, incl 33AA gliadin peptide
  • gliadin is deamidated in mucosa by tissue transglutaminases (tTG)
  • in those w/ HLA-DQ2 and HLA-DQ8 haplotypes, deamidated gliadin closely fits the MHC II grooves
  • gliadin presented to T helper cells by antigen presenting cells
  • initiates a Th2-predominant immune response
  • generates cytotoxic T cells against gliadin
  • cytotoxic T cells migrate into intestinal epithelium, visible on biopsy as intraepithelial lymphocytes
  • the T cells damage + destroy epithelial cells resulting in progressive villous atrophy
  • as a result, crypts become hyperplastic to compensate for cell loss
  • loss of normal small bowel fxn -> malabsorption
  • also a humoral immune response w/ generation of antigliadin, antiendoymysial and antiTTG antibodies - useful antibodies diagnostically
85
Q

What is the clinical presentation of coeliac disease?

A
  • at any age, most commonly in childhood or middle age
  • symptoms of malabsorption (diarrhoea, steatorrhoea, weight loss, lethargy, bloating, abdo pain)
  • non-specific symptoms: eg. anaemia (usually iron def), irritable bowel syndrome-like symptoms, altered bowel habit, abdo pain
  • in children, coeliac disease is an important cause of failure to thrive and delayed puberty
  • an intensely itchy and blistering rash over elbows + buttocks - dermatitis herpetiformis
  • some pts are asymptomatic and diagnosis is discovered incidentally
86
Q

How is coeliac disease diagnosed?

A
  • history and examination
  • gluten-containing diet better to be consumed during diagnostic process
  • serology tests: total IgA and IgA tissue transglutaminase antibodies are currently the preferred first line test (owing to its high sensitivity and negative predictive value)
  • IgA anti-endomysial (EMA) antibodies can be used if IgA tTG is weakly positive
  • gold standard ix: endoscopy and duodenal biopsy
87
Q

What does tissue biopsy for positive coeliac show?

A
  • villous atrophy
  • crypt hyperplasia
  • prominent intraepithelial lymphocytes

Generally agreed that duodenal biopsy should be performed on all adult patients to confirm the diagnosis

88
Q

What is the treatment for coeliac?

A
  • Life-long gluten-free diet
  • Those with coeliac disease (+ fam members, carers) should be given sources of info on the disease, including a national and local specialist coeliac groups and dietiticans with a specialist knowledge of coeliac disease
89
Q

What are complications of coeliac disease?

A
  • Malabsorption (-> anaemia + deficiencies)
  • Osteopenia/osteoporosis
  • Dermatitis herpetiformis
  • Lymphoma
90
Q

Why do patients with coeliac develop osteopenia/osteoporosis? How can this be investigated and treated?

A
  • most pts w/ coeliac disease are osteopenic (reduced bone density)
  • bc they fail to reach their peak bone mass during young adult life
  • due to malabsorption of calcium
  • reduction in bone density is usually mild, most pts are only osteopenic
  • however, some are actually osteoporotic w/ associated risk of fracture
  • at dx, pts given lifestyle advice + basline DEXA scan to assess bone mineral density
  • pts should maintian adequate calcium and vit D intake
  • a gluten-free diet should prevent further bone loss and may improve bone density
91
Q

Why do coeliac patients develop dermatitis herpetiformis?

A
  • intensely itchy chronic blistering skin condition
  • typically occurs symmetrically on extensor surfaces (buttocks, back of neck, knees, elbows etc)
  • it’s not related to herpes virus
  • rather, associated w/ coeliac disease although exact mechanism not fully understood
  • may be due to autoantibodies to epidermal transglutaminase

*Medicine: Cellular Pathology (16 decks)

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