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Year 3 > Week Ten - Case One > Flashcards

Week Ten - Case One Flashcards

1
Q

what is the second most common cancer worldwide

A

gastric adenocarcinoma

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2
Q

what is the male to female ratio of gastric adenocarcinoma

A

2:!

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3
Q

what is the cause of gastric adenocarcinoma thought to be

A

the combination of genetic factors and nitrates in the diet, with increased risk on smokers and those with h pylori infection

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4
Q

what is diagnosis usually a combination of

A

usually a combination of an endoscopy and CT +/- USS

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5
Q

what is staging of gastric adenocarcinoma done using

A

the TNM scale

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6
Q

what are gastric tumours almost always

A

almost always an adenocarcinoma of the mucous secreting cells of gastric pits. the most common mutation is that of tumour suppressor gene p53

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7
Q

what is the 5 year syrivival rate of stomach cancer

A

about 10%

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8
Q

what are the two other types of tumours that affect the stomach

A

Gastric lymphoma (MALT) – accounts for 1-2% of gastric carcinomas.
H pylori is again a large precipitating factor. Presentation often similar to gastric adenina carcinoma and thus may be difficult to differentiate from GORD or gastric ulcer

Oesophageal carcinoma – almost always occurs in the presence of Barrett’s oesophagus, and is basically just an adenocarcinoma of the new columnar epithelium – i.e. it is similar historically to gastric carcinoma. Likely to present with dysphagia

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9
Q

what sort of diets can predispose you to gastric adenocarcinoma

A

smoked fish, pickled foods, salt and nitrates

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10
Q

what foods have a beneficial benefit

A

fresh fruit and vegetables, particular those containing vitamin C and A

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11
Q

what is thought to be responsible for 60-70% of gastric adenocarcinoma s

A

h pylori

you are at greater risk of you get the infection when you are young, and if you are one of the people who goes hypocholorohydric when they get it

H pylori will often cause inflammation, leading to gastritis, leading to gastric atrophy, which leads to gastric carcinoma

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12
Q

what are the other risks for developing gastric adenocarcinoma

A

Smoking
Gastric polyps
FAP (familial adenomatous polyposis)
Genetic factors – e.g. HDC-1 mutations
Resection of the stomach

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13
Q

what are the symptoms of gastric adenocarcinoma

A

History of recent dyspepsia.(50%) This pain will be very similar to that of peptic ulcer disease, and can often be relieved by antacids.
Loss of appetite / anorexia (35%)
Bloating / fullness
Weight loss (72%)
Vomiting/nausea (40%)
Iron-deficiency anaemia due to occult bleeding
Dysphagia (22%)
Melaena (20%)
Mass (17%)
Haematemesis is unusual

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14
Q

what are the red flag symptoms

A

patients of any age, with dyspepsia, AND
- chronic GI bleeding
- dysphagia
- progressive wright loss
- iron deficiency anaemia
- perisitent vomtiing
- epigastric mass
- suspicious barium meal result

OR

patients > 55
- with sudden onset dyspepsia

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15
Q

what are the tests done to confirm gastric adenocarcinoma

A

essentially all you need to do is a gastroscopy and routine FBC, and LFTs

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16
Q

what is the most common genetic factor for gastric adenocarcinoma

A

loss of the TSG p53 which occurs in about 70% of gastric cancersw

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17
Q

where are early gastric cancers confined to

A

the mucosa and the submucosa, whilst more advanced cancers can penetrate the muscular proproria, and may become ulcerating

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18
Q

what is the prognosis for early gastric cancer

A

90%

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19
Q

how can the cancers be described

A

as either intestinal or diffuse

intestinal ones have histology representative of internal epithelium, whilst diffuse ones arise form normal gastric mucosa

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20
Q

who do diffuse cancers tend to occur in

A

younger patients

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21
Q

what is the pattern of the disease

A

initially there will be chronic gastritis leading to atrophy, then onto metaplasia, and premalignant dysplasia, finally ending up at malignancy

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22
Q

where can gastric cancer spread lymphatic ally to

A

the Virchow’s node, and can spread via venous blood to the liver and ovaries

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23
Q

what are Krukenburg tumours

A

spread of cancer via the venous blood to the liver and ovaries

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24
Q

what will a CT show

A

liver metastasis, but not lymph node involvement. will also show gastric wall thickening

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25
Q

what will an endoscopic ultrasound show

A

how far the tumour has progressed through the gastric wall and lymph node involvement

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26
Q

what is the other way to stage gastric tumours apart from TNM

A

UICC score

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27
Q

what is the best form of treatment

A

surgery is the best form of treatment

28
Q

what does this surgery involve

A

a partial or total resection of the stomach, and removal of varying amounts of surrounding lymph nodes

29
Q

what are the only treatments available for those who surgery is not available to

A

only palliative care, pain relief and counselling are available

30
Q

what are the early complications of surgery

A

usually respiratory, cardiac and wound complications

leakage at the point of anastomosis, particularly if it was a total gastrectomy, and the oesophagus is joint straight onto the jejunum

fluid collection and accesses around areas of lymph node dissection

acute pancreatitis if lymph nodes form this region have been removed

nasogastric drainage if the jejunum doesn’t drain well after the operation

31
Q

what are the features of late complications of surgery usually

A

these are normally due to physiological changes in the upper GI tract. most of these will appear within a few months of surgery, but then disappear within a year

32
Q

what are the actual late complications of surgery

A

Reflux gastritis due to loss of the pyloris and reflux of biliary contents into the stomach. Most patients who have surgery will have endoscopic evidence of gastritis, but only a small percentage will have significant symptoms.

Dumping – is a term used to refer to many symptoms that are attributed to rapid gastric emptying. These symptoms include:
Fullness
Pain
Nausea
Diarrhoea
Vomiting

Vasomotor symptoms – i.e. the symptoms affecting the level of dilatation of the blood vessels. These are due to rapid fluid shifts into the bowel lumen, and are similar to the symptoms of hypovolaemia. Hypovolaemia is a decreased blood volume.

Late dumping – this is due to an insulin surge soon after a meal followed by reactive hypoglycaemia.
Dumping is treated by controlling the diet. Patient’s should eat lots of small meals, keep dry food and liquids separate, and avoid simple sugars. The symptoms of dumping will lessen over time.

Weight loss – Patients who have a total gastrectomy will lose about 10% of their body weight, whilst those who have a partial gastrectomy will only lose about 5%. This is due to a combination of factors, including, symptoms of dumping, change in diet, gastritis, and possibly due to continuing cancer progression.

Anaemia – very common as a result of loss of intrinsic factor due to the fact you have removed the parietal cells in the stomach! Another factor will also be that iron remains in its insoluble ferric form, as there may not be enough acid to convert it to ferrous. After a total gastrectomy, patients have to have vitamin B12 injections.

Increased risk of osteoporosis and osteomalacia – it is not entirely clear why this is the case, but it is possibly to do with reduced calcium / vitamin D absorption

33
Q

what is one of the most common indications for palliative care

A

gastric outlet obstruction from a stenosing distal gastric cancer, but there are many others

34
Q

what is the median life expectancy for somebody just diagnosed with incurable gastric cancer

A

4-6 months

it is very important that a palliative plan is put in place as soon as possible after diagnosis

35
Q

what percentage of all gastric neoplasms does gastric lymphoma account for

A

2-5%

36
Q

where do gastric lymphomas occur

A

in the mucosa associated lymphoid tissue (MALT)

this type of tissue appears in the stomach as a result of chronic inflammation, which is thought to be a result of h pylori infection

37
Q

is MALT tissue normally present in the stomach

A

NO

38
Q

the lymphomas are normally ? cell derived?

A

normally B cell derived although T cell ones do sometimes occur

39
Q

how can these gastric lymphomas be classified

A

as high or low grade

low grade tumours are treated with H pylori eradication treatment, and this’ll also result in healing of the tumour in 70-100% of cases

high grade tumours are treated with chemoradiotherapy

40
Q

what is Murphy’s sign

A

this is pain in the right upper quadrant from local peritoneum from acute cholecysitits

41
Q

what is a paraumbilical hernia

A

a paraumbilical hernia should present with a lump around the umbilicus. there may be skin changes over this lump if there are incarcerated contents within the hernia

42
Q

what is Cullens sign

A

this is periumbilical ecchymosis

43
Q

what is Caput Medusae

A

these are periumbilical varies that branch out from the umbilicus that occurs with portal hypertension from liver cirrhosis

44
Q

what is Rovsing’s sign

A

this is pain felt in the right iliac fossa on palpation in the left iliac fossa from local peritoneum from acute appendicitis

45
Q

what is Grey-Turner’s sign

A

ecchymosis in either flank

46
Q

what do Cullen’s and Grey-Turner’s sign both indicate

A

internal haemorrhage which can present in acute pancreatitis, splenic rupture or perforatied peptic ulcer disease

when these signs result from acute haemorrhagic pancreatitis, this can indicate severe disease and higher mortality

47
Q

what is acute pancreatitis

A

is an inflammation of the pancreas caused by an activation of pancreatic enzymes and autodigestion

it can often cause a SIRS which in turn can cause organ failure such as AKI, and respiratory failure

48
Q

how is acute pancreatitis diagnosed

A

a diagnosis requires at least 2 of the following 3 features;
- abdominal pain
- serum lipase/amylase levels greater than 3 times the upper limit of normal
- radiological evidence of pancreatitis

49
Q

what is more sensitive, lipase or amylase

A

lipase

Amylase rises rapidly within 2 hours of the onset of acute pancreatitis, and peaks between 12 and 72 hours. It is then excreted rapidly by the kidneys, with levels returning to normal as soon as 3 days. Lipase, however, peaks at 24 hours and can remain elevated for between 8 and 14 days as it is reabsorbed by the renal tubules back into the circulation. This biochemical profile makes lipase a much better clinical test for acute pancreatitis.

50
Q

what is the description of mild acute pancreatitis

A

no organ failure or local/systemic complications

51
Q

what is the description of moderate severe acute pancreatitis

A

transient organ failure such as AKI, resolving within 48 hours

may have local complication

52
Q

what is the description of severe acute pancreatitis

A

persistent organ failure or multi organ failure

53
Q

what are the two types of acute pancreatitis

A

interstitial oedematous pancreatitis and necrotising pancreatitis

54
Q

what is the most common type of pancreatitis

A

interstitial oedematous pancreatitis

pancreatic parenchyma is inflamed or oedematous

55
Q

what does interstitial oedematous pancreatitis lead to

A

acute peripancreatic fluid collection (APFC)

occurs within 4 weeks, the fluid is extra pancreatic in location

if not resolved within 4 weeks, it may organise and become a pseudocyst

56
Q

what is a pseudocyst

A

a homogenous fluid filled collection with a cyst wall

can compress on surrounding structures, such as the stomach

57
Q

what is necrotising pancreatitis

A

necrosis of the pancreatic parenchyma and or peripancreatic tissue

may become infected

58
Q

what does necrotising pancreatitis lead to

A

acute necrotic collection (ANC)

occurs within 4 weeks. the fluid is intra or extra pancreatic in location

inhomogeneous collection of fluid and solid components

no wall

59
Q

what is walled off necrosis (WON)

A

occurs after 4 weeks of onset of pain

60
Q

what are the causes for acute pancreatitis

A

ERCP
alcohol
gallstone disease
autoimmune diswase
family history
idiopathic
high serum triglyceride levels

61
Q

what criteria is used to diagnose acute pancreatitis

A

Atlanta criteria

62
Q

what does the Atlanta criteria state

A

that the patent should have two of the following to diagnose acute pancreatitis ;

  1. epigastric pain
  2. raised lipase/amylase
  3. radiological evidence of acute pancreatitis
63
Q

once diagnosis has been established, what is the next most appropriate investigation in patients pathway of acre

A

ultrasound of the abdomen

Investigations should focus firstly on establishing the diagnosis. If the diagnosis at admission is at all unclear, then a CT scan would be warranted to rule out any other pathology. A CT for acute pancreatitis within the first week correlates very poorly with clinical severity, as is its sensitivity for diagnosing necrotising pancreatitis within the first few days. CT imaging is most useful 5-7 days after hospital admission, as this is the timeframe for when local complications may develop.

An US Abdo is therefore the next appropriate investigation for the patient. Although he has a clear risk factor (i.e., high alcohol intake), gallstone disease accounts for over 50% of acute pancreatitis cases and needs to be ruled out as a cause. An US is the investigation of choice for this.

64
Q
A
65
Q

w

A

Year 3 (63 decks)

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