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Scientific Basis of Clinical Practice > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

describe the structure of the oesophagus

A

lined by squamous mucosa
separated from the submucosa by the muscularis mucosa
deep to this; muscularis propria, with the inner circular and outer longitudinal bundles of smooth muscle

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2
Q

describe the conditions involving oesophageal stenosis

A

congenital stenosis/atresia; generally paediatric, associated with fistula

thoracic oesophageal malignancy; rarely fistulae into the trachea or one of the main bronchi, frequently leading to mediastinitis and sepsis

achalasia; rare, dysmotility of the distal oesophagus causes dilatation of the proximal oesophagus, can precipitate infection, inflammation and epidermoid metaplasia, can predispose to squamous carcinoma of the oesophagus

liver cirrhosis and elevation of venous pressure in portal venous circulation; engorgement and dilatation of the vascular channel at sites of portal systemic anastomosis, can precipitate oesophageal varices formation
bleeding and haematemesis

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3
Q

describe oesophagitis

A

most common cause is reflux oesophagitis
cause; regurgitation of the gastric contents into the lower oesophagus
results from incompetence of the lower oesophageal sphincter
symptoms; heartburn, water brash, odynophagia

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4
Q

what are the complications of oesophagitis?

A

ulceration and necrosis of the squamous epithelial lining; acute inflammation
stricture and stenosis; repeated long-term acute inflammation
fibrosis and structuring; chronic inflammation
Barrett’s metaplasia

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5
Q

describe Barrett’s oesophagus

A

the stratified squamous epithelial lining is replaced by a columnar epithelial lining/mucosa in the distal 1/3rd of the oesophagus
endoscopy; appears red and velvety vs white native squamous mucosa
can only be detected by endoscopy
histology; squamous mucosa replaced by mate plastic intestinalised columnar mucosa

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6
Q

describe candidal infection of the oesophagus

A

often seen in immunosuppressed patients; diabetes, HIV, AIDS
endoscopy; raised white plaques
microscopy; fungal hyphae, can be accentuated using periodic acid shift

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7
Q

describe herpes oesophagitis

A

linear, punched out ulcers within the oesophagus
microscopy; viral infection, multinucleate squamous epithelial cells, containing ground glass viral inclusions
particularly seen in leukaemia and lymphoma
associated with odynophagia

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8
Q

describe eosinophilic oesophagitis

A

common in young adult males
often present with dysphagia
concentric rings; trachealisation of the oesophagus/feline oesophagus
histology; numerous eosinophils within the squamous epithelium
eosinophilia in the peripheral blood
increased serum try-taste
eosinophilic infiltrates in other parts of the GI tract

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9
Q

describe the different types of cancer of the oesophagus

A

squamous carcinoma; commonest in middle 1/3, commonest in Asia and Iran
adenocarcinoma; comment in distal 1/3, particularly prevalent in obese middle-aged caucasians
more common in males

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10
Q

what are the risk factors for squamous carcinoma of the oesophagus?

A 
alcohol
tobacco
dietary nitrosamines
types of fungi
achalasia
genetic predisposition; tylosis
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11
Q

what are the risk factors for adenocarcinoma of the oesophagus?

A

GORD
obesity/body habitus
barrett’s oesophagus
alcohol/tobacco

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12
Q

what are the patterns of oesophageal cancer?

A

necrotising malignant ulcer eroding into the wall or adjacent structures
exophytic, polypoid luminal mass
3 diffuse infiltrative neoplasms resulting in stricture

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13
Q

describe Barrett’s metaplasia/oesophagus

A

a pre-malignant condition
risk factor for oesophageal adenocarcinoma
patients are followed by endoscopic surveillance to detect pre-malignant dysplastic change

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14
Q

what is the treatment of dysplastic Barrett’s tissue?

A

can be destroyed by an endoscopic procedure
insertion of a radio frequency ablation device and ablating the abnormal mucosa
only destroys to a depth of a few hundred micrometers
insufficient to treat early cancers

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15
Q

describe endoscopic mucosal resection

A

can treat early Barrett’s related oesophageal adenocarcinoma with a low risk of nodal metastasis
but 90% of oesophageal adenocarcinomas present with advanced disease

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16
Q

describe the staging of oesophageal carcinoma

A

T1; confined to the innermost layers of the wall
pT1a; intramucosal disease, have not breached the muscularis mucosa
T3; break through the muscularis propria into the surrounding oesophageal adventitial fat
N1 etc; nodal involvement

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17
Q

describe the presentation of oesophageal carcinoma

A

most common; pT3N1
dysphagia
weight loss
may have occult metastatic disease; PET scan

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18
Q

what is the treatment of oesophageal carcinoma?

A

dependent on stage
early lesions; endoscopic mucosal resection
more advanced; oesphagectomy
pT3N1; neoadjuvant chemotherapy, then surgery
middle 1/3 tumours and showing squamous morphology; radical chemoradiation
surgically incurable; palliative chemotherapy
HER2 positive; trastuzumab
very unwell; palliative stenting

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19
Q

describe acute erosive gastritis

A

small punctuate areas of erosion and inflammation in the gastric mucosa
seen in endoscopy

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20
Q

what are the causes of acute erosive gastritis?

A 
NSAIDs
iron tables
alcohol
corrosive substance ingestion
systemic chemotherapy
uraemia; CKD
shock; widespread burns
sepsis
recent major surgery
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21
Q

what are the types and causes of chronic gastritis?

A

type A; autoimmune gastritis, associated with pernicious anaemia and lymphocytic infiltrate within the gastric mucosa
type B; chronic active gastritis due to h. pylori infection
type C; distinctive pattern of mucosal injury and regenerative change associated with the exposure of the gastric mucosa to certain types of chemical, NSAIDs, alcohol

most common cause; reflux of bile or duodenal contents
seen sporadically or in previous gastric surgery

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22
Q

describe h. pylori infection

A

gram negative rod shaped organism
results in chronic active inflammation
secretes urease, breaks down urea to ammonia, resulting in local pH buffering, allowing bacteria to survive
certain strains also produce cytotoxins and incite and inflammatory reaction in the mucosa
can be tested with the ammonia breath test at endoscopy

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23
Q

what are the complications of helicobacter infection?

A 
chronic active gastritis
peptic ulcers; gastric and duodenal
corpus gland atrophy
intestinal metaplasia
gastric carcinoma
gastric lymphoma
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24
Q

what are the features and complications of peptic ulcers?

A

haematemesis; coffee grounds
perforation
scarring and stenosis of pylorus; pyloric outlet obstruction

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25
Q

what are the types of gastric carcinoma?

A

intestinal type

diffuse/poorly cohesive type

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26
Q

describe the intestinal type gastric carcinoma

A

neoplastic cells form glandular structures that are readily appreciable
particularly prone to lymphovascular invasion and haematogenous spread
more liver metastases seen

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27
Q

describe the diffuse/poorly cohesive type gastric carcinoma

A

single cell pattern, single dispersed cancer cells infiltrate between and around pre-existing gastric mucosal gland structures
tumour cells adopts a signet ring cell morphology
may diffusely infiltrate and involve the stomach wall
the stomach loses its normal functional ability and becomes rigid
more peritoneal cavity spread; krukenberg tumours

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28
Q

what are the clinical features of gastric carcinoma?

A 
asymptomatic
weight loss
epigastric mass
haematemesis
vomiting
virchow's node; metastasis to the supraclavicular lymph node
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29
Q

describe krukenberg tumour

A

spread through the peritoneum to involve the ovaries and give rise to bilateral ovarian metastases

30
Q

describe the diagnosis and treatment of gastric carcinoma

A

laparscopy with peritoneal washings; detection of peritoneal metastases
malignant cells in the fluid; contraindication to surgery
removal at primary site is futile if it has spread to the peritoneal cavity

31
Q

describe gastric lymphoma

A

longstanding h. pylori chronic gastritis can result in lymphoid follicle formation and accumulation of mucosa associated lymphoid tissue; MALT
antigen-dependent polyclonal reactive lymphoid proliferation
can progress to low-grade lymphoma

32
Q

what are the histological features of gastric lymphoma?

A

confluent patterns of growth of the follicles
destruction of the pre-existing native gastric mucosal glands by the formation of lymphoepithelial lesions
associated with monoclonality

33
Q

what is the treatment of gastric lymphoma?

A

h. pylori eradication sometimes causes regression of the lymphoid infiltrate
antibiotics
cytotoxic chemotherapies
surgery
conventional lymphoma treatment; spread from another histological type of lymphoma
conventional anti-lymphoma treatment; primary gastric marginal zone lymphoma, primary gastric lymphoma, secondary lymphoma

34
Q

describe GI stromal tumours

A

mesenchymal spindle cell tumours
most commonly found in the stomach and the small bowel
dumbbell configuration
sometimes ulceration in relation to the overlying gastric mucosa
seen clearly on CT
difficult to obtain diagnostic preoperative biopsies; ulcer slough

35
Q

what are the consequences of GI stromal tumours?

A

mostly small, benign and incidental findings
larger; can be associated with haemorrhage and haematemesis, behave more aggressively
small bowel; more aggressive, behave more malignantly
malignancy; can spread through the peritoneal cavity and develop liver metastases
uncommon to metastasise to local regional lymph nodes

36
Q

describe CD 117 or c-kit expression of GI stromal tumours

A

tyrosine kinase gene mutation
susceptible to imatinib (selective TKI)
also show exon 11 of KIT gene mutations

37
Q

what tumours can affect the small bowel?

A 
adenocarcinoma
carcinoid tumours
GI stromal tumours
malignant lymphoma
metastases
38
Q

describe small bowel adenocarcinoma

A

less common than primary colonic adenocarcinoma; may be metastatic spread
mostly sporadic
commonly duodenal; napkin ring stricture
associated with crohn’s and coeliac disease
often presents late with poor prognosis

39
Q

describe duodenal tumours

A

may be associated with FAP

often polypoid

40
Q

what are the common sites of primary colonic adenocarcinoma metastases?

A

small bowel
lung
ovary
breast

41
Q

describe the grading of carcinoid tumours

A

1; low-grade malignant tumours, usually primary appendices carcinoids
3; morphological overlap with small cell carcinoma or large cell neuroendocrine

42
Q

describe carcinoid syndrome

A

the release of serotonin/5-hydroxytryptamine into the systemic circulation
via the hepatic vein from liver metastases
facial flushing
sweating
wheezing
diarrhoea
long term; endocardial fibrosis in tricuspid and pulmonary valves, associated with RSHF

43
Q

how is carcinoid syndrome diagnosed?

A

urinary 5-hydroxyindoleacetic acid (5-HIAA) levels

octreotide or somatostatin scan

44
Q

what syndromes are carcinoid tumours associated with?

A

Zollinger-Ellison syndrome; hypergastrinaemia, carcinoid tumour in the 1st part of the duodenum
hypergastrinaemia; peptic ulceration
MEN-1

45
Q

describe the histological features of carcinoid syndrome

A

cells with granular eosinophilic cytoplasm
monotonous, low grade features of malignancy
insular or trabecular pattern in a fibrovascular stroma, can sometimes contain amyloid

46
Q

describe GI stromal tumours of the small bowel

A

less common
more aggressive
c-KIT mutations; imatinib
exon 9 of KIT gene mutations; implications for blockade of TK with imatinib

47
Q

describe malignant lymphoma of the small bowel

A

common site; 25-30% of GI lymphomas

may be primary or secondary

48
Q

what are the types of malignant lymphoma of the small bowel?

A

MALToma
Burkitt’s lymphoma
follicular lymphoma
mantle cell lymphoma
enteropathy associated T cell lymphoma (EATL)
post transplant lymphoproliferative disorder

49
Q

describe MALToma of the small bowel

A

associated with h. pylori infection

represent a form of low-grade B-cell non-hodgkin’s lymphoma

50
Q

describe Burkitt’s lymphoma

A 
relatively uncommon
high-grade B-cell non-Hodgkin's lymphoma
associated with EBV
associated with immunosuppression
common in children and young adults
frequently seen in the terminal ileum
very chemo-responsive
51
Q

describe folicular lymphoma

A

low-grade B-cell non-hodgkin’s lymphoma
frequently in mesenteric lymph nodes
can occur as a primary neoplasm, particularly within the duodenum

52
Q

describe mantle cell lymphoma

A

very strongly associated with the GI tract
usually involves the colon
can form multiple polypoid masses, resulting in multiple lymphomatous polyposis
intermediate grade B-cell lymphoma

53
Q

describe enteropathy associated T-cell lymphoma (EATL)

A

aggressive, high-grade, T-cell, non-hodgkin’s lymphoma
very strongly associated with the jejunum and ileum
can be associated with coeliac disease
refractory coeliac disease; prodromal syndrome or a pre-malignant condition

54
Q

describe post-transplant lymphoproliferative disorders

A

associated with immunosuppression; treatment of IBD
EBV-driven disorder
most common in renal and other transplants

55
Q

describe metastases of the small bowel

A

relatively common
more common that metastases to the large bowel
primary sites; lung, ovary, stomach, breast carcinoma, metastatic melanoma
lobular carcinoma of the breast; most common breast carcinoma that metastasises to the small bowel, also involves the mesentery and retroperitoneum

56
Q

describe polyps

A

raised lesion within the lumen of the GI tract
arises within the wall
often pre-malignant
most common types; hyper plastic and adenomatous
hamartomatous polyps; can occur as an inherited polyposis syndrome, Peutz Jeghers syndrome or juvenile polyposis

57
Q

describe hyperplastic polyps

A 
very common
very little malignant potential
appear as small polypoid lesions
often on the folds of mucosa
show serrations; localised hyperplasia of the colonic mucosa
58
Q

describe adenomatous polyps

A

very common
dysplastic; indicated an increased risk of malignancy
can range from a few mm to several cm
predominately tubular or villous architecture

59
Q

what features of a polyp indicate malignancy?

A

size
degree of dysplasia
type; tubular polyps have a lower risk of dysplasia than those with a villous projection

60
Q

describe serrated polyps

A

hydra between the hyperplastic and adenomatous polyp
do not show the same conventional type of dysplastic change that is seen in adenomatous polyps
have pre-malignant potential

61
Q

describe FAP

A

AD inheritance
mutation of the APC gene on the long arm of chr 5
growth of many hundreds of adenomatous polyps throughout the large bowel
increased chase of developing colorectal carcinoma

62
Q

what is the management of carcinoma within the polyp?

A

invasive adenocarcinoma in a pedunculated polyp; endoscopic snare polypectomy
sessile adenomatous polyps; difficult to remove because of mechanical reasons and because they may be associated within invasion of the wall and earlier spread

63
Q

what are the identifiable causes of colorectal adenocarcinomas?

A

10% in total;
5%; HNPCC/Lynch syndrome, results in genetic micro-satellite instability
2%; history of IBD, particularly UC (those with severe UC ~10yrs will have sclerosing cholangitis)

64
Q

describe the adenoma carcinoma sequence

A

a morphologically defined progressive sequence of changes associated with tumour development and progression
can be associated with increasing numbers of molecular abnormalities, mutations within tumour suppressor genes and and oncogenes

65
Q

describe the vogelstein model of the adenoma carcinoma sequence

A 
normal epithelium
dysplastic ACF
early adenoma
late adenoma
cancer
metastatic cancer
66
Q

describe the presentation of right-sided colon tumours

A

iron deficiency anaemia; ulcerating tumour causing blood loss over a prolonged period of time

67
Q

describe the presentation of left-sided colon tumours

A

change in bowel habit
crampy abdominal pain
intestinal obstruction; solid stool, thicker wall, smaller lumen

68
Q

what investigations are required to stage a colorectal cancer?

A

MRI; rectal cancer staging
CT chest, abdomen and pelvis; nodal status, examine the liver
serum CEA; useful in following the progress of a tumour in patients receiving oncological treatment

69
Q

what is the treatment of colorectal cancer?

A

surgery; removal of the segment of bowel affected, associated with the relevant anatomical lymph node drainage groups
adjuvant chemotherapy; to prolong disease-free survival in node positive patients
radiotherapy; primarily for rectal cancer, used prior to surgery or in combination with chemotherapy

70
Q

describe rectal tumour surgery

A

mesorectal excision margin; extraperitoneal middle and distal 1/3 of the rectum
all of the tissue is removed en bloc
prevention/reduction of the indigence of local/pelvic recurrence of rectal adenocarcinoma

71
Q

describe the non-surgical rectal tumour treatment

A

more bulky and advanced; incomplete tumour resection and recurrence
pre-operative radiotherapy
short course radiotherapy
combination chemotherapy and radiotherapy
long course chemoradiotherapy

Scientific Basis of Clinical Practice (10 decks)

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