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YR3 Gastro > Stomach conditions > Flashcards

Stomach conditions Flashcards

1
Q

What is the commonest type of stomach cancer?

A

Most tumours are adenocarcinomas.

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2
Q

Define stomach cancer

A

Neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs.

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3
Q

What genes can be involved in gastric cancer?

A

Gastric cancer can involve loss of the tumour suppression gene, p53

Several proto-oncogenes, such as ras, c-myc, and erbB2 (HER2/neu), have been shown to be over-expressed in gastric cancers

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4
Q

Explain some risk factors for gastric cancer

A
  • Pernicious anaemia (2-3x increased risk)
  • Helicobacter pylori-
    • bacteria cause inflammation, which can result in atrophy, metaplasia, and carcinoma.
  • Smoked and processed foods, foods high in nitrosamines, high nitrates, high salt, pickling, low vitamin C
  • smoking
  • family history
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5
Q

Summarise the epidemiology of gastric cancer

A
  • COMMON cause of cancer death worldwide
  • Higher incidence in East Asia (esp Japan), Eastern Europe, and South America
  • 6th most common cancer in the UK
  • Usual age of presentation: > 50 yrs
  • 2x more frequent in men
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6
Q

Recognise the presenting symptoms of gastric cancer

A

Weight loss and persistent abdominal pain are the most common presenting symptoms

Other symptoms:

  • Nausea, early satiety
  • Dysphagia (in tumours of the gastric cardia)
  • Lower GI bleeding → meleana, haematemesis, symptoms of anaemia
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7
Q

Recognise the signs of gastric cancer on physical examination

A

Abdominal tenderness may be noted - tends to be epigastric and vague in early-stage disease.

An abdominal mass may be present in patients with advanced disease.

Lymphadenopathy may also be present in advanced disease:

  • left supraclavicular node (Virchow’s node)
  • periumbilical nodule (Sister Mary Joseph’s nodule)
  • left axillary node (Irish node)
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8
Q

Name the 2 tumours that commonly result from gastric cancer metastases

A
  • Krukenberg’s Tumour (ovarian metastases)
  • Sister Mary Joseph’s Nodule (malignant metastatic umbilical nodule)
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9
Q

Identify appropriate investigations for gastric cancer

A
  1. Upper GI endoscopy with biopsy + histology
    • establish diagnosis
    • all ulcers
  2. Endoscopic ultrasound
    • stageing
  3. CXR + CT
    • to detect metastatic lesions
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10
Q

What is the main DDx for gastric cancer? How would you distinguish between the two?

A

Peptid ulcer disease

Distinguished from gastric neoplasm by endoscopy and biopsy.

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11
Q

Differentiate between, and define, PUD and gastritis

A

Gastritis is generalised, PUD is localised

PUD = a break in the mucosal lining of the stomach or duodenum >5 mm in diameter, with depth to the submucosa.

Gastritis = histological presence of gastric mucosal inflammation.

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12
Q

Where are peptic ulcers most commonly located?

A

Most commonly gastric and duodenal

(but they can also occur in the oesophagus and Meckel’s diverticulum).

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13
Q

Describe the aeitiology of gastric ulcers

A

Peptic ulcers result from an imbalance between factors:

  • promoting mucosal damage
    • gastric acid
    • pepsin
    • Helicobacter pylori infection
    • NSAID use
  • promoting gastroduodenal defense
    • prostaglandins
    • mucus
    • bicarbonate
    • mucosal blood flow
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14
Q

State some common causes of PUD/gastritis

A
  • Helicobacter pylori infection
  • NSAID use
  • bisphosphonates
  • smoking
  • increasing age
  • Hx/FHx
  • Zollinger-Ellison syndrome (rare)
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15
Q

What is Zollinger-Ellison syndrome?

A

Condition in which:

  • a gastrin-secreting tumour or
  • hyperplasia of the islet cells in the pancreas

cause overproduction of gastric acid, resulting in recurrent peptic ulcers

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16
Q

Summarise the epidemiology of PUD/gastritis

A

Common

Mean age:

  • Duodenal ulcer: 30s
  • Gastric ulcers: 50s

Epidemiology largely reflects the epidemiology of the two major aetiologic factors:

  • Helicobacter pylori infection
  • use of NSAIDs
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17
Q

Recognise the presenting symptoms of both peptic ulcer disease and gastritis

A

Most common presentation:

  • dyspepsia
  • chronic or recurrent post-prandial epigastric pain
  • Relieved by antacids

Other symptoms:

  • eg haemetemesis, melaena (→anaemia)
  • anorexia
  • Nausea, relieved by eating.
  • Vomiting occurs after eating.
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18
Q

Describe how you can diffferentiate between epigastric pain of a gastric vs duodenal ulcer

A

Gastric -

  • pain is worse soon after eating

Duodenal -

  • pain is worse several hours after eating
  • pain may be severe and radiate through to back as a result of penetration of the ulcer posteriorly into the pancreas.
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19
Q

in terms of aetiology, how do gastric and duodenal ulcers differ?

A

duodenal = 90% H. pylori, 10% NSAID use

  • There is an increase in acid in the duodenum

gastric = 65% H.pylori, 35% NSAID use

  • There is a decrease in protective mucus
  • NSAIDs = COX1 inhibitor
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20
Q

Recognise the signs of peptic ulcer disease and gastritis on physical examination

A

There may be NO physical findings

  • Epigastric tenderness
  • ‘pointing’ sign- patient can localise pain with one finger
  • Signs of complications e.g. anaemia (ulceration into the gastro-duodenal artery)
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21
Q

Identify appropriate investigations for peptic ulcer disease and gastritis

A

If < 55 and no red flags

  • H pylori breath test/stool antigen test
  • FBC
  • Stool occult blood test
  • Serum gastrin- if there are multiple duodenal ulcers

If > 55 / red flags present / treatment fails

  • Upper GI endoscopy and biopsy
  • Histology+ urease testing are performed on stomach biopsies obtained during endoscopy. (no biopsy for duodenal)
  • If ulcer is present: repeat endoscopy 6-8 weeks after treatment to confirm resolution and exclude malignancy
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22
Q

What are the red flags in suspected PUD?

A
  • weight loss
  • bleeding/melaena
  • anaemia
  • early satiety
  • dysphagic
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23
Q

Briefly explain the 4 possible tests that can be done for H. Pylori

A
  1. Urea breath test:
    • Radio-labelled (C13) urea is given by mouth
    • CO213 is detected in the expelled air
  2. Blood antibody test
    • IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
  3. Stool antigen test
  4. Campylobacter-like organism (CLO) test:
    • Gastric biopsy is placed with a substrate of urea and a pH indicator
    • If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
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24
Q

What test would you perform if you suspected Zollinger-Ellison syndrome?

A

Secretin test

IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients

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25
Q

Generate a management plan for ACUTE, bleeding PUD/gastritis

A
  1. Endoscopy + blood transfusion/fluid resuscitation ​​
    • identify + stop bleeding (adrenaline)
  2. PPI
    • patients with upper GI bleeding should be treated with IV PPIs at presentation until the cause of bleeding is identified
    • esomeprazole: 80 mg intravenous bolus given over 30 minutes
  3. surgery or embolisation via interventional radiology
    • where endoscopic haemostasis of bleeding ulcers fails
26
Q

How should you treat a H. Pylori negative PUD/gastritis?

A

Treat underlying cause

  • PPI (omeprazole- oral) for 4-8 weeks

OR

  • H2 antagonist (famotidine)
27
Q

How should you treat a H. Pylori positive PUD/gastritis?

A

Triple therapy (1-2 weeks)- combination of 2 antibiotics + PPI:

  • omeprazole oral
  • clarithromycin oral
  • amoxicillin/metronidazole
28
Q

How should you treat PUD caused by NSAID use?

A

Stop NSAID use

Use misoprostol (prostoglandin E1 analogue) if NSAID use is necessary

(plus PPIs)

29
Q

Identify the possible complications of peptic ulcer disease and gastritis

A

Rate of major complication = 1 % per year

Major complications:

  • Haemorrhage (haematemesis, melaena, iron-deficiency anaemia)- ulcer erodes into the wall of a gastroduodenal blood vessel.
  • Perforation (erect CXR, NBM, IV Abx)- ulcer erodes into peritoneum
  • Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)
30
Q

Summarise the prognosis for patients with peptic ulcer disease and gastritis

A

Overall lifetime risk = 10%

Outlook is generally good because peptic ulcers associated with H. pylori can be cured by eradication

31
Q

Define gastrointestinal perforation

A

Perforation of the wall of the GI tract with spillage of bowel contents

32
Q

State some causes of GI perforation in the large bowel

A

Common:

  • Diverticulitis
  • Colorectal cancer
  • Appendicitis

Others:

  • volvulus
  • ulcerative colitis (toxic megacolon)
33
Q

State some causes of GI perforation in the small bowel (RARE)

A
  • Trauma
  • Infection (e.g. TB)
  • Crohns
34
Q

State some causes of GI perforation in the stomach and oesophagus

A

Oesophagus:

  • Boerhaave’s perforation - transmural rupture of the oesophagus following forceful vomiting
  • Mallory-weiss tear

Gastroduodenal:

  • Perforated duodenal or gastric ulcer
  • gastric cancer
35
Q

Recognise the presenting symptoms of gastrointestinal perforation

A

All present with sudden onset, severe abdominal pain

Generalised and is worse on movement

  • Malignancy - may have accompanying weight loss and nausea/vomiting
  • If oesophageal- neck/chest pain and dysphagia
36
Q

Recognise the signs of gastrointestinal perforation on clinical examination

A
  • Very UNWELL
  • Signs of shock
  • Pyrexia
  • Pallor
  • Dehydration
  • Signs of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds)
  • Loss of liver dullness (due to overlying gas)
37
Q

Identify appropriate investigations for gastrointestinal perforation

A
  1. Bloods:
    • FBC, U&E – urea raised after upper GI bleed, LFTs
    • Amylase - will be raised with perforation (but should not be astronomical (as seen in pancreatitis))
  2. Erect CXR
    • ​​would show pneumoperitoneum
  3. AXR
    • Shows abnormal gas shadowing
  4. Gastrograffin Swallow
    • For suspected oesophageal perforations
38
Q

Generate a management plan for gastrointestinal perforation- MEDICAL

A
  • NBM
  • Fluid/electrolyte resuscitation
  • IV Abx with anaerobic cover (cefuroxime. metronidazole)
39
Q

Generate a management plan for gastrointestinal perforation- SURGICAL

A

Peritoneal lavage plus:

Oesophageal:

  • (pleural lavage as higher up)
  • Surgical repair

Gastroduodenal:

  • Laparotomy - repair using a peritoneal patch
  • biopsy any tumours/ulcers

Large bowel:

  • Hartmann’s procedure
  • Surgical resection of the rectosigmoid colon with closure of the anorectal stump and formation of an end colostomy.
40
Q

Identify possible complications of gastrointestinal perforation

A

Large and Small Bowel - peritonitis

Oesophagus - mediastinitis, shock, overwhelming sepsis and death

41
Q

Summarise the prognosis for patients with gastrointestinal perforation

A

Gastroduodenal

  • Gastric ulcers = >M+M than duodenal
  • POOR prognosis for perforated gastric carcinomas

Large Bowel

  • High risk of faecal peritonitis if left untreated
  • This can lead to DEATH from septicaemia and multiorgan failure
42
Q

Define gastroenteritis

A

Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.

43
Q

What pathogens can cause gastroenteritis?

A
  • viruses
  • bacteria
  • protozoa
  • toxins contained in contaminated food or water (faecal-oral route)
44
Q

State some organisms that are responsible for dyssentry

A

CHESS:

  • Campylobacter jejuni
  • Haemorrhagic E Coli O157
  • Entamoeba histolytica
  • Salmonella
  • Shigella
45
Q

What is a common cause of gastroenteritis in the elderly on Abx?

A

C. Difficile

46
Q

State some commonly contaminated foods and the organisms responsible

A
  • Improperly cooked meat – S.aureus, C. perfringens
  • Old rice – B cereus, S aureus
  • Eggs and poultry - Salmonella
  • Milk and cheeses – Listeria, Campylobacter
  • Canned food – Botulinism
47
Q

Summarise the epidemiology of gastroenteritis

A

COMMON- 20% UK population/anum

Diarrhoeal disease remains a leading cause of mortality worldwide.

Most deaths are in young children in developing countries.

48
Q

Recognise the presenting symptoms of gastroenteritis

A

Acute onset nausea, vomiting, diarrhoea

DIARRHOEA

  • watery diarrhoea = viral
  • bloody diarhoea = dyssentry (non-viral)

Other symptoms:

  • fever
  • abdominal pain and cramping

other effects of toxins:

  • Botulinum causes paralysis
  • Mushrooms can cause fits, renal or liver failure
49
Q

How does the onset of symptoms give an indication of the cause of gastroenteritis?

A

Toxins = early (1-24 hours)

Bacterial/viral/protozoal = 12+ hour

50
Q

Recognise the signs of gastroenteritis on physical examination

A
  • Abdomen should be soft and only mildly tender.
    • If there is pain and guarding, investigate other diagnoses
    • e.g. pancreatitis, appendicitis, IBD
  • Abdominal distension
  • Bowel sounds are often INCREASED
  • Fever
  • Signs of volume depletion:
    • dry mucous membranes
    • tachycardia
    • hypotension
    • decreased urine output
    • weight loss
51
Q

What is important to consider when a patient presents with gastroenteritis?

A

Gastroenteritis is usually self-limiting but can cause serious illness due to dehydration and electrolyte imbalance in the:

  • very young
  • old
  • immunocompromised

Need to evaluate for signs of dehydration and assess whether urgent fluid resuscitation is needed.

52
Q

List some systemic symptoms and signs of dehydration on examination

A

Symptoms:

  • Thirst
  • Decreased urine output
  • Dry mucous membranes; check tongue and mouth
  • Altered mental state; drowsiness.

On examination:

  • SBP <100 mmHg
  • HR >90bpm
  • Cold peripheries
  • RR >20
  • NEWS >5
53
Q

Identify appropriate investigations for gastroenteritis

A

Bloods:

  • FBC
  • urea and electrolytes
  • creatinine
  • blood culture (identify bacteraemia)

Stool for culture, ova, and parasites

  • stool viral culture
  • analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin)

If other, non-pathogenic cause suspected:

  • AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)
  • Sigmoidoscopy- uneccessary except to exclude IBD
54
Q

Generate a management plan for gastroenteritis

A

Initial management

Assess hydration status. Initial treatment is to prevent or treat dehydration:

  • Fluid and electrolyte replacement with oral rehydration solution
  • IV rehydration- patients with signs of shock or severe dehydration/if severe vomiting

Supplemental treatment

  • Antibiotics - only used if severe/infective agent identified
  • Bed rest – should stay at home until D+V cleared for 48h
55
Q

What are the 3 key treatment goals for gastroenteritis?

A
  • Prevent and treat volume depletion
  • Maintain nutrition
  • Reduce transmission of the virus to other people.
56
Q

How would you treat gastroenteritis caused by botulinium toxin?

A

If botulism is present (due to Clostridium botulinum) treat with botulinum antitoxin (IM) and manage in ITU

NOTE: notifiable disease and an important public health issue

57
Q

How would you treat gastroenteritis caused by C. Difficile?

A
  • Isolate
  • Oral metronidazole 10-14 days
  • If refractory: vancomycin
58
Q

Identify the possible complications of gastroenteritis

A
  • Dehydration
  • Electrolyte imbalance
  • Prerenal failure
  • Secondary lactose intolerance (particularly in infants)
  • Sepsis and shock
59
Q

Which pathogens can be responsible for:

  • Guillan-Barre syndrome
  • HUS
  • Paralysis of respiratory muscles
A
  • Guillan-Barre syndrome*- may occur weeks after recovery from Campylobacter gastroenteritis
  • HUS*- associated with toxins from E. coli O157
  • Paralysis of respiratory muscles*- botulism
60
Q

Summarise the prognosis for patients with gastroenteritis

A

Good prognosis because most cases are self-limiting

61
Q
A

YR3 Gastro (12 decks)

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