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Pathology Upper GI Flashcards

1
Q

What is the J line?

A

The gastro-oesophageal junction

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2
Q

What type of epithilium lines the oesophagus?

A

Stratified squamous epithilium

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3
Q

What can be found in the submucosa of the oesophagus?

A

Submucosal glands which secrete mucin to protect the oesophagus

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4
Q

Acute oesophagitis is rare. What cases it?

A

Corrosive agents following injection

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5
Q

What can cause acute oesophagitis in immunocomprimised patients?

A

Candida, herpes, CMV

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6
Q

Chronic oesophagitis is common. What is the most common cause?

A

Reflux disease- reflux oesophagitis

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7
Q

What are the rare causes of chronic oesophagitis?

A

Crohn’s disease

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8
Q

What is reflux oesophagitis?

A

Inflammation of the oesophagus due to refluxed low pH gastric content

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9
Q

What causes reflux oesophagitis?

A

1) Defective sphincter mechanism/ hiatus hernia
2) Abnormal oesophageal motility
3) Increased intra-abdominal pressure (obesity and pregnancy)

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10
Q

What are the microscopic changes in reflux oesophagitis?

A

Basal zone expansion and lengthening of papillae due to increased desquamation
Intraepithilial neutrophils, lymphocytes and eosinophils (small numbers)

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11
Q

Increase replication leads to a greater chance of mutation. T or F?

A

True

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12
Q

What are some of the complications of reflux oesophagitis?

A

Ulceration and bleeding (if the epithilium cannot regenerate fast enough)
Strictures(due to fibrosis following inflammation => narrowing and dysphagia
Barretts Oesophagus

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13
Q

What is Barrett’s oesophagus?

A

Replacement of stratified squamous epithilium of the oesophagus with columnar epithilium of the stomach. Metaplasia due to stress

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14
Q

What causes Barrett’s oesophagus?

A

Persistent reflux of acid or bile => expansion of columnar epithilium from gastric glands or from submucosal glands.
Protective response

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15
Q

Can differention from oesophageal stem cells cause barrett’s oesophagus?

A

Yes. The differentiated cells do not change its the new cells which differentiate differently

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16
Q

How does Barretts’s oesophagus appear macroscopically?

A

Red velvetty mucosa replacing the normal mucosa

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17
Q

What are the microscopic chages in Barrett’s oesophagus?

A

Looks like stomach and small bowel.

Has goblet cells wich produce musin to protect the oesophagus from the acid and enzymes

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18
Q

What are the complications of Barrett’s oesophagus?

A

Increased risk of developing dysplasia and carcinoma of the oesophagus. Unstable mucosa

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19
Q

How is barrett’s oesophagus managed?

A

Medically and surveillance/screening although the value is disputed

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20
Q

What are the greatest risk factors for adenocarcinoma and squamous cell carcinoma of the oesophagus?

A

Adenocardinoma= acid reflux

Squamous cell carcinoma = Smoking and drinking

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21
Q

What is allergic oesophagitis?

A

Eosinophilic oesophagitis. Inflammation of the oesophagus due to to an allergen. NOT due to acid reflux

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22
Q

Who gets allergic oesophagitis?

A

Both children and adults.
Males more than females
Those with a personal or family history of atopy or asthma

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23
Q

What are the signs of allergic oesophagitis?

A

Increased eosinophils in the blood and biopsy tissue

Corrugated or spotty oesophagus. Looks like the trachea

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24
Q

What is the treatment for allergic oesophagitis?

A

Steroids, chromoglycate, montelukast

Will not respond to PPIs or surgery

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25
Q

What type of tumours are commonly found in the oesophagus?

A

Benign = rare
Malignant = more common
Majority are primary tumours rather than secondary tumours which have invaded the oesophagus

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26
Q

What is the most common benign tumour of the oesophagus?

A

Squamous papilloma
Rare, assymptomatic and HPV related.
Wart on the epithilium

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27
Q

What are the common malignant tumours?

A

Squamous cell carcinoma (more common in males) and adenocarcinoma

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28
Q

What are the causes/risk factors for squamous cell carcinoma?

A 
Smoking, Alcohol
Vitamin A/Zinc deficiency
HPV
Oesophagitis 
Genetic
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29
Q

What are the complications of oesophageal cancers?

A

Dysphagia,

Ulceration

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30
Q

What are the microscopic changes in squamous cell carcinoma?

A

Keratin pearls

Dysplasia

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31
Q

What are the risk factors fro adenocarcinomaof the oesophagus?

A

Male
Obesity => GORD
Most common in the western world and in the lower 1/3rd of the oesophagus

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32
Q

If someone presents with dysphagia, what should you do?

A

Endoscopy and biopsy

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33
Q

Why is it important to differentiate adino carcinoma from squamous cell carcinoma?

A

Effects targeted therapies

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34
Q

What are the mechanisms of metastates or cancer spread?

A

Direct invasion
Lymphatic permiation
Vascular invasion

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35
Q

Why are lymph node metastates common in oesophageal carcinoma?

A

Because there is a chain of lymph nodes along the oesophagus and stomach surface

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36
Q

What is the 5 year survival of oesophageal cancer?

A

5-10%

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37
Q

Where does oesophageal cancer often spread to in the blood stream?

A

Liver

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38
Q

How may oesophageal cancer present?

A

Dysphagia- red flag. Due to tumour obstruction

General symptoms of malignancy if they present with spread- Anaemia, weight loss, lethargy

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39
Q

What ia a Mallory Weiss tear and what causes it?

A

Superficial tear in the oesophagus often due to sustained and prolonged vomiting increasing pressure.

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40
Q

What are oesophageal varices and what causes them?

A

Dilated veins in the oesophageal mucosa caused by portal hypertension and liver disease

41
Q

What is the most common cancer of the mouth?

A

Squamous cell carcinoma

42
Q

What are the high risk sites for oral cancer?

A

Floor of mouth, lateral and ventral surfaces of the tongue, soft palate, retromolar pad and tonsillar pillars

43
Q

What are the risk factors for oral cancers?

A

Smoking, alcohol, HVP, chronic infections, Patient with history of primary oral SSC is at an increased risk of a second primary.

44
Q

What are the microscopic changes in oral squamous cell carcinoma?

A

Swirls and keratin pearls, dysplasia, local invasion and destruction of local tissues

45
Q

How is progonisis of oral cancer determined?

A

Tumour stage and how much can be surgically excised

46
Q

What is the treatment for oral cancer?

A

Surgery +/- chemo or radio

47
Q

What is the 5 year survival of oral cancer?

A

40-50%

Not improved over the last few decades despite improvements in treatment. Need to detect earlier

48
Q

What causes acute gastritis?

A 
Irritant chemical injury
Severe trauma (shock, burns, head injury) Blood supply is directed away from the stomach elsewhere but can lead to ischemia and inflammation
49
Q

What are the causes of chronic gastritis?

A

ABC
Autoimmune
Bacterial
Chemical

50
Q

What are the rare inflammatory disorders of the stomach?

A

Lymphocytic, eosinophilic, granulomatous

51
Q

What are the macroscopic signs of chronic gastritis?

A

Red inflamed stomach

52
Q

What causes autoimmune chronic gastritis?

A

Immune system produces antibodies against stomach cells and products.
Anti-parietal and anti-intrinsic factor antibodies.
Causes atrophy and intestinal metaplasia
in the body of the stomach

53
Q

What are the consequences of autoimmune chronic gastritis?

A

Pernicious anaemia, macrocytic (RBCs are larger than their normal volume) due to a Vitamin B 12 deficiency.
Increases risk of malignancy

54
Q

Why do patients with autoimmune gastritis get a vitamin B 12 deficiency?

A

Because Intrinsic factor (produced by parietal cells) are attacked by auto antibodies. Intrinsic factor is required for uptake of Vitamin B12

55
Q

What is SACDC?

A

Subacute combined degeneration of spinal cord.

56
Q

Why do patients with autoimmune chronic gastritis get SACDC?

A

Vitamin B12 is required to produce myelin and without this the nerves of the spinal cord degenerate.
Effects walking and balence

57
Q

What are some of the histological changes you may see in autoimmune chronic gastritis?

A

Intestinal metaplasia of the stomach
Enlarged and hypersegmented RBCs due to macrocytic anaemia
Pallor in columns of the back due to the lack of myelin around the nerves

58
Q

What causes bacterial chronic gastritis (most common type)?

A

H.pylori
urvive in the surface mucus slime of the stomach and irritate the epithilium to excite an inflammatory response. Initially acute and then chronic if the bacteria is not cleared.

59
Q

Describe H pylori and what is the most critical inflammatory

mediator that it provokes?

A

Gram negative curvilinear rod

Interlukin 8

60
Q

H. pylori gastritis increases the risk of other conditions. WHat are these?

A

Duodenal ulcers
Gastric ulcers
Gastric carcinoma
Gastric lymphoma

61
Q

What are the causes of chemical chronic gastritis and how does this occur?

A

Alcohol, bile reflux and NSAIDs

Direct injury o mucus layer by fat solvents

62
Q

What are the histological signs of chemical gastritis?

A

Epithilial regeneration, hyperplasia, congestion and little inflammation. Cna produce erosions or ulcers

63
Q

What is peptic ulceration?

A

A breach in the gastrointestinal mucosa as a result of acid and pepsin attack. Its a form of chronic inflammation of the stomach.

64
Q

Why are peptic ulcers so difficult to heal?

A

Lots of acid and enzymes in the environment. Can become chronic

65
Q

What are the common sites for chronic peptic ulcers?

A

Duodenum (1st part) gets regularly insulted with acidic chyme.
Stomach (junction of body and antrum
Gastro-oesophageal junction
Stromal ulcers

66
Q

What causes chronic duodenal ulcers?

A

Many causes
50% have increased acid secretion
Many have sustained acid secretion following a meal
Excess acid in the duodenum => gastric metaplasia and h ylori infection causing inflammation, epithilial damage and ulceration.

NB: There is also a failure of host defence

67
Q

What do peptic ulcers look like macroscopically?

A

Edges are clear cut and punched out
2-10cm across
Transversely the ulcer is a depressed area and the muscle layer is thickened drawing in the rugae

68
Q

What are the microscopic changes seen in peptic ulcers?

A

Layered appearance
Floor of necrotic, fibronopurulent debris
Base of inflamed granulation tissue
Deepest layer is fibrotic scar tissue- This will contract, eventually leading to a stricture

69
Q

What are the complications of peptic ulcers?

A

Perforation, Penetration, Haemorrhage, Stenosis and irretractable pain. Can errode into other organs and blood vessles

70
Q

What are the benign tumours found in the stomach?

A

Hyperplastic polyps
Cystic fundic gland polyps
Easliy removed at endoscopy

71
Q

What are the malignant tumours found in the stomach?

A

Carcinomas (mainly adenocarcinomas)
Lymphomas
Gastrointestinal Stromal tumours (GISTs) rare

72
Q

Where are the highests incidences of gastric adenocarcinomas?

A

Japan, China, Columbia and Finland (diet of smoked fish)

Where H pylori is more prevalent

73
Q

Where is the most common site for gastric andenoma?

A

Cardia, gasto-oesophageal junction

74
Q

Patients with anit-h.pylori antibodies have a higher incidence of gastric adenocarcinoma. T or F?

A

True

75
Q

What is the pathogenisis of gastric adenocarcinoma?

A 
H pylori infection (damages cells => increased replication and mutation)
Chronic gastritis 
Intestinal metaplasia/atrophy
Dysplasia
Adenocarcinoma
76
Q

What other cnditions, apart from h pylori infection, can predispose you to gastric adenocarcinoma?

A

Pernicious anaemia
Partial gastrectomy (lower half of stomach removed inc. pyloric sphincter => chronic duodenal reflux of bile)
Lynch sydrome
Menetrier’s disease

77
Q

What is Lynch syndrome

A

Lynch syndrome is an autosomal dominant genetic condition that has a high risk of colon and gastric cancer as well as other cancers including endometrial cancer

78
Q

What is Menetrier’s disease?

A

a rare, acquired, premalignant disease of the stomach characterized by massive gastric folds, excessive mucous production with resultant protein loss, and little or no acid production.

79
Q

What are the 2 sub types of gastric adenocarcinoma?

A

Intestinal type- exophytic/ well defined

Diffuse- expands and infiltrates the stomach wall

80
Q

How can you tell malignant ulcers from benign peptic ulcers?

A

Maligant ulcers do not look uniform and the epithilium is reflected up so it looks like a creator

81
Q

What do adenocarcinomas produce?

A

Glands

Signet rings sometimes

82
Q

Why do diffuse adenocarsinomas of the stomach have a worse prognosis than intestinal adenocarcinomas?

A

Diffuse are harder to surgically resect.

15% are mixed and this is very hard to treat

83
Q

How do gastric adenomas spread?

A

Local invasion- other organs and peritoneal cavity and ovaries.
Lymph nodes
Haematogenous - to the liver

84
Q

What is a kruckenberg tumour?

A

A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.

85
Q

What is a maltoma?

A

Gastric lymphoma derived from mucosa associated lymphoid tissue (MALT)

86
Q

Is maltoma associated with H pylori infection?

A

Yes and sometimes if you treat the h pylori infection the maltoma will disappear

87
Q

How does a Maltoma develop?

A

Continuous inflammation induces an evolution into clonal B cell proliferation- low grade. B cells attack the gastric epithilium.
If unchecked can evolve into a high grade B cell lymphoma

88
Q

What is the prognosis of gastric cancer?

A

Pretty poor. Worse than oesophageal cancer

89
Q

What is the treatment for resectable oesophageal cancer?

A

Pre surgery chemo/radio
Laproscopic oesophagectomy
Post surgery chemo/radio.
This is similar for gastric cancer

90
Q

What oesophageal cancers are found in the Western world and the Eastern world and what are the risk factors?

A 
West = adenocarcinoma. reflux due to obesity 
East = Squamous cell carcinoma due to smoking, alcohol and hot tea.
91
Q

What is the difference between melena and haematochezia?

A

Haematochezia is passage of bright red blood with stool.

Melena is black stools due to digested blood

92
Q

What does bloods with a raised urea and normal creatinine mean?

A

The patient is digesting blood

93
Q

What is Beorhaave?

A

Spontaneous rupture of the lower oesophagus

94
Q

What does vomiting coffee coloured blood mean?

A

The blood has sat in the stomach for a while and been oxidised before vomiting- sign of gastric cancer

95
Q

What is the prognosis for oesophageal cancer?

A

50% 5 year survival

96
Q

What is the commonest cause of dysphagia?

A

Stroke

97
Q

What is the treatment for oesophageal cancer if it is unresectable?

A

Stenting for dysphagia and possible palliative chemo/radiotherapy

98
Q

Does adenocarcinoma respond to radiotherapy well?

A

Not really- squamous cell cancer responds well but with adencarcinoma you have to use chemo.

GI (48 decks)

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