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GSSE Pathology > Pathology - Gastro > Flashcards

Pathology - Gastro Flashcards

0
Q

What is the most common form of congenital intestinal atresia?

A

Imperforate anus.

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1
Q

Which type of oesophagotracheal fistulae is the most common?

A

Type C; where there is a blind ending proximal oesophagus and a distal tracheo-oesophageal fistula.

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2
Q

What is the difference between Omphalocoele and Gastroschisis?

A

In Gastroschisis all layers of the abdominal wall (peritoneum to skin) fail to develop.

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3
Q

What is the most common site for gastric mucosa ectopia?

A

The proximal oesophagus.

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4
Q

Features of a Meckel’s diverticulum?

A

A true congenital diverticula as a result of persistence of the vitellointestinal duct. 2% of the population; males are twice as affected. Heterotopic gastric or pancreatic tissue may be present. The former can cause ulceration.

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5
Q

Brief overview of pyloric stenosis?

A 
1:500 births M:F 4:1
Associated with Turners and trisomy 18
Presents with projectile vomiting within 3 weeks
Palpable "olive"
Cured with full thickness myotomy.
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6
Q

Brief overview of Hirschsprung Disease?

A

1:5000 live births
A result of arrested migration of neural crest cells into the gut yielding an aganglionic segment. The rectum is always affected.
Genetic component, variable penetrance.

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7
Q

What is Plummer Vinson Syndrome?

A

A triad of:
Oesophageal webs
Iron deficiency anaemia
Glossitis

Is a risk factor for oesophageal SCC

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8
Q

Primary achalasia is idiopathic. What are some causes of secondary achalasia?

A

Chagas’ disease
(Vagal dorsal nuclei) polio, surgery
Autonomic neuropathy
(Infiltrative) Amyloidosis, malignancy

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9
Q

What is Barrett Oesophagus?

Frequency?
Implications?

A

A complication of GORD characterised by intestinal metaplasia within the oesophageal squamous mucosa.

Occurs in 10% of GORD
Pre-invasive dysplasia is detected in ~2% each year.

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10
Q

What are the two most common causes of oesophageal varices?

A

Alcoholic cirrhosis

Hepatic schistosomiasis

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11
Q

Brief description of oesophageal adenocarcinoma:

A

Largely evolve from Barrett Oesophagus with 7:1 male predilection. Account for around half of oesophageal cancers. Has a stepwise genetic pathogenesis.

Typically involves distal third. Usually detected at advanced stage so 5-year survival is less than 25%.

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12
Q

Brief description of oesophageal SCC:

A

Age >45 with a 4:1 male predilection.
Risk factors include EtOH and tobacco, PVS, caustic injury, achalasia, and scalding beverages!

Half of O.SCC occurs in middle third. Rich lymphatic network promotes spread. Overall 5 year survival is 9%.

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13
Q

Describe the NSAID related pathogenesis of gastritis:

A

NSAIDS block COX and thereby reduce the protective effect of prostaglandin. Bicarbonate production is also reduced.

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14
Q

Curling versus Cushing ulcers?

A

Curling ulcers occur in the proximal duodenum in associated with burns or trauma (stress)

Cushing (gastric, duodenal, oesophageal) ulcers occur in association with intracranial disease. Acid hypersecretion is thought to be due to direct vagaries stimulation. They have a high risk of perforation.

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15
Q

Virulence factors for H. pylori?

A

Motility with flagella
Urease production
Bacterial adhesins
Toxins (cagA and vagA)

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16
Q

Diagnostic tests for H. pylori?

A 
Antibody serology
Urea breath test
Bacterial culture
Bacterial visualisation
DNA based tests.
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17
Q

H. pylori is a risk factor for?

A

Gastric adenocarcinoma
Gastric B cell lymphoma
Peptic ulcer disease.

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18
Q

What is the pathogenesis of autoimmune gastritis?

A

CD4 T cell mediated destruction of parietal cells is the major pathogenic mechanism.

Antibodies to IF and parietal cells are SECONDARY!

Achlorhydia then triggers hypergastrinaemia and antral G-cell hyperplasia. Pernicious anaemia is manifest.

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19
Q

Brief description of Zollinger Ellison syndrome:

A

Caused by gastrin secreting tumours. Typically arise in SB or pancreas. Elevated gastrin levels (up to 5-fold) aid diagnosis.

Mostly sporadic but in ~25% they are associated with MEN type 1. 60-90% are malignant gastrinomas

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20
Q

Gastric polyps:

3 Types
Malignant potential?

A 
Inflammatory and Hyperplastic polyps:
75% of gastric polyps
Occur between ages 50-60
Associated with chronic gastritis
Polyps >1cm should be removed. 
Gastric adenomas:
10% of gastric polyps
Associated with gastritis and FAP
30% harbour carcinoma
>2cm are particularly concerning.

Fundic polyps:
In women >50 or in FAP

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21
Q

Brief description of Gastric adenocarcinoma:

A

20 times more common in Japanese, Eastern Europe, Chile and Costa Rica.

Diet and H. pylori and lack of AO are risk factors.

Loss of intracellular adhesion is a key step in oncogenesis.

Prognosis depends on stage: surgical resection gives 90% but overall 5-year survival is 30%.

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22
Q

What germline mutation is associated with familial gastric carcinomas and 50% of sporadic lesions?

A

Mutations in the CDH1 gene encoding for E-cadherin.

p53 mutations are also present in the majority of cancers.

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23
Q

Where do gastric cancers typically occur?

A

Gastric cancers involve the antrum more than the lesser curvature which is more affected than the greater curvature.

24
Q

Prognosis in gastric cancer depends on what factors?

A

Depth of invasion

Extent of nodal spread or distal metastases.

25
Q

Most MALTomas are what type of cancer?

A

Marginal zone B cell lymphoma.

26
Q

What features characterise carcinoid syndrome?

A

Cutaneous flushing
Bronchospasm
Increased bowel motility
Right sided cardiac valve thickening.

27
Q

Why does carcinoid syndrome affect only 10% of patients with gastrointestinal carcinoid?

A

Because of hepatic metabolism of the carcinoid products.

28
Q

Brief description of carcinoid tumours:

A

Peak incidence is in the 6th decade of life.
Carcinoid are usually slow growing, indolent, malignancies, and symptoms are largely a function of the hormones produced.

Prognosis depends on site of the the primary:
Foregut tumours rarely metastasise and resection is curable
Midgut tumours are usually multiple and aggressive
Hind gut tumours are usually only found incidentally, though colonic rulers can be large and metastasise.

29
Q

Brief description of GISTs:

A

Peak incidence in 60’s
Increased incidence in patients with NF1 and in girls with Carney triad.

Arise from interstitial cells of Cajal
75-80% of GISTs contain oncogenes gain of function c-KIT mutations.

Non-resectable tumours can be treated with Imatinib

30
Q

What is the pathogenesis of Coeliac disease?

How can we test for it?

A

Gliadin induces epithelial IL-5 expression with local activation and proliferation of CD8 cytotoxic cells that drive enterocyte apoptosis.

The most sensitive serological test is IgA antibodies to tissue transglutaminase or IgG/IgA to deaminated gliadin.

31
Q

Cholera toxin does what?

A

Opens CF transmembrane conductance regulator (via cAMP) and releases chloride ions into the lumen.

Massive obligate diarrhoea and dehydration then occur.

32
Q

What is the most common cause of childhood diarrhoea?

A

Rotavirus

Adenovirus is the second most common.

33
Q

Compare and contrast the macroscopic features of Crohn’s disease and ulcerative colitis:

A

Ulcerative colitis is limited to the colon, Crohn’s may affect any part of the GI tract.
Ulcerative colitis has a diffuse distribution compared to the skip lesions seen in Crohn’s.
There is often wall thickening in Crohn’s due to the transmutation inflammation, whereas the wall in UC is relatively unaffected.
Strictures are common in SB Crohn’s, dilation is common in UC.

34
Q

Compare and contrast the microscopic features of Crohn’s disease and ulcerative colitis:

A

Both conditions are characterised by chronic mucosal damage with blunting of the crypts and dysphasia.

The hallmarks of Crohn’s are transmural inflammation, non-caseating granulomas and fistulae/sinuses. These are not present with UC.

35
Q

Compare and contrast the clinical features of Crohn’s disease and ulcerative colitis:

A

Perianal fistulae may occur in Crohn’s, not UC.
Fat malabsorption only occurs in Crohn’s.
Toxic megacolon may occur in UC, not Crohn’s.
There is malignant potential in both (with colonic Crohn’s)

36
Q

What are the extra-intestinal features of Crohn’s and UC?

A 
Migratory polyarthritis
Sacrioiliitis
Ankylosing spondylitis 
Erythema nodosum
Uveitis
Cholangitis
Amyloidosis (type AA)

Primary sclerosing cholangitis may occur in up to 7.5% of UC.

37
Q

What are the “non-neoplastic” polyps of the large bowel?

A
  1. Hyperplastic polyps (90% of epithelial intestinal polyps)
  2. Hamartomatous polyps
    • Juvenile polyps
    • Juvenile polyposis syndrome (can become adenomas..!).
    • Peutz Jeghers syndrome (at risk of multiple Ca!)
38
Q

What is Peutz Jeghers syndrome?

Why is it important to recognise?

A

A syndrome characterised by multiple gastrointestinal hamartomatous polyps and mucocutaneous hyperpigmentation.

These patients are at higher risk of several cancers including colon, pancreas, breast, lung, gonad, and uterus.

39
Q

What are the “neoplastic” polyps of the large bowel?

A

Colonic adenomas are benign polyp precursors to the majority of CRC; they are characterised by the presence of epithelial dysplasia. Incidence is 50% at 50 years.

Most are benign, risk of malignancy correlates with size and degree of dysplasia:
Polyps >4cm have a 40% risk of malignancy.

40
Q

What dysplastic changes might be seen in adenomatous polyps?

A

Hyperplasia
Nuclear hyperchromasia
Loss of polarity

41
Q

Why do INTRAmucosal carcinomas have little metastatic potential compared to invasive adenocarcinomas?

A

Intramucosal carcinomas lack access to lymph channels.

42
Q

Brief description of Familial Adenomatous Polyposis:

A

FAP is an autosomal dominant disorder caused by mutations of the APC gene.

Patients in adolescence will typically develop more than 100 colonic adenomatous polyps; if untreated CRC will develop in 100% by the age of 30.

43
Q

Does prophylactic colectomy prevent gastrointestinal cancer in patients with FAP?

A

No. While prophylactic colectomy prevents colorectal cancer from occurring, these patients also develop adenomas in the stomach and ampulla of Vater.

44
Q

What are the variants of FAP?

A

Gardner syndrome = Multiple osteomas, epidermal cysts, duodenal and oesophageal cancers, fibromatosis, and abnormal dentition.

Turcot syndrome = FAP plus medulloblastomas

Attenuated FAP = Fewer polyps (~30). Cancer risk ~50%

45
Q

What is the APC gene?

A

Adenomatous Polyposis Coli gene is found on chromosome 5q21

Normal APC function promotes cell adhesion and regulates proliferation.

Absence of APC function leads to decreased cell adhesion and increased cell proliferation.

46
Q

Brief description of HNPCC:

A

HNPCC is an autosomal dominant familial disorder also known as Lynch syndrome.

It is characterised by an increased risk of CRC and extraintestinal cancer, particularly of the endometrium. Adenomas occur in low numbers and considerably earlier than the general population.

The hallmark of HNPCC is mutations in DNA repair genes leading to microsatellite instability.

47
Q

What is microsatellite instability?

A

Microsatellite are tandem repeats of 1-6 nucleotides scattered throughout the genome.

Microsatellite sequences of an individual are fixed for life and are the same in every tissue.

With errors in mismatch repair, there are expansions and contraction of these sequences in tumour cells, creating alleles not found in the normal cells of the same patient.

Such defects leave the individual exposed to a second oncogenic hit…

48
Q

What are the epidemiological risk factors for CRC?

A

Diet: high in fat and CHO, low in vegetable fibre.

Diminished antioxidants: Vitamins A, C, and E

NSAIDS are protective: inhibit PGs which promote growth.

49
Q

Brief description of Colorectal Adenocarcinoma:

A

Peak incidence is between 60-79.
Rectal Ca has a 2:1 M:F ratio. This bias is not present more proximally.

The most important prognostic indicator is stage at presentation.

50
Q

What is the most common tumour of the appendix?

A

Carcinoid. The appendix is the most common site of gut carcinoid followed by the small intestine.

51
Q

What are the most common derivative sources for peritoneal metastases?

A

Ovarian and pancreatic cancer.

52
Q

What are the two primary tumours of the peritoneum?

A

Mesothelioma and Desmoplastic Small Round Cell Tumour.

53
Q

Which three features correlate strongly with malignant risk of polyps?

A

Polyp size
Histological architecture
Severity of epithelial dysplasia.

54
Q

What are the types and frequencies of polyp epithelial architecture?

A 
Tubular adenomas (90%)
Villous adenomas (1%)
Tubulovillous adenomas (5-10%)
55
Q

Signet ring cells are associated with which malignancies?

A 
Prostate
Bladder
Colon
Breast
Gastric
Testicular
Ovarian stroma
Gallbladder
56
Q

What is the organism most commonly associated with anaerobic infections of the gut?

A

Bacteroides fragilis.

57
Q

What is the treatment for Bacteroides fragilis?

What is it resistant to?

What are its pathogenic features?

A

Meteonidazole, Carbapenams, various cephalosporins.

Resistant to beta lactams and increasing resistance to Clindycin.

Capsule resists phagocytosis so triggers abscess formation.

GSSE Pathology (17 decks)

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