Stomach conditions Flashcards
1
Q
What is the commonest type of stomach cancer?
A
Most tumours are adenocarcinomas.
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.
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
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
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
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
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)
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)
9
Q
Identify appropriate investigations for gastric cancer
A
-
Upper GI endoscopy with biopsy + histology
- establish diagnosis
- all ulcers
-
Endoscopic ultrasound
- stageing
-
CXR + CT
- to detect metastatic lesions
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.
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.
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).
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
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)
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
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
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.
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.
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
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)
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
22
Q
What are the red flags in suspected PUD?
A
- weight loss
- bleeding/melaena
- anaemia
- early satiety
- dysphagic
23
Q
Briefly explain the 4 possible tests that can be done for H. Pylori
A
-
Urea breath test:
- Radio-labelled (C13) urea is given by mouth
- CO213 is detected in the expelled air
-
Blood antibody test
- IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
- Stool antigen test
-
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
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
25
Generate a management plan for ACUTE, bleeding PUD/gastritis
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
How should you treat a H. Pylori **negative** PUD/gastritis?
Treat underlying cause
* **PPI (omeprazole- oral) for 4-8 weeks**
OR
* H2 antagonist (famotidine)
27
How should you treat a H. Pylori positive PUD/gastritis?
Triple therapy (1-2 weeks)- combination of 2 antibiotics + PPI:
* **omeprazole** oral
* **clarithromycin** oral
* **amoxicillin/metronidazole**
28
How should you treat PUD caused by NSAID use?
Stop NSAID use
Use **misoprostol** (prostoglandin E1 analogue) if NSAID use is necessary
(plus PPIs)
29
Identify the possible complications of peptic ulcer disease and gastritis
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
Summarise the prognosis for patients with peptic ulcer disease and gastritis
Overall lifetime risk = **10%**
Outlook is generally good because peptic ulcers associated with **H. pylori can be cured by eradication**
31
Define gastrointestinal perforation
Perforation of the wall of the GI tract with spillage of bowel contents
32
State some causes of GI perforation in the large bowel
Common:
* **Diverticulitis**
* **Colorectal cancer**
* **Appendicitis**
Others:
* volvulus
* ulcerative colitis (toxic megacolon)
33
State some causes of GI perforation in the small bowel (RARE)
* Trauma
* Infection (e.g. TB)
* Crohns
34
State some causes of GI perforation in the stomach and oesophagus
_Oesophagus:_
* **Boerhaave's perforation** - transmural rupture of the oesophagus following forceful vomiting
* **Mallory-weiss tear**
_Gastroduodenal:_
* Perforated **duodenal or gastric ulcer**
* **gastric cancer**
35
Recognise the presenting symptoms of gastrointestinal perforation
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
Recognise the signs of gastrointestinal perforation on clinical examination
* **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
Identify appropriate investigations for gastrointestinal perforation
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
Generate a management plan for gastrointestinal perforation- MEDICAL
* NBM
* **Fluid/electrolyte** resuscitation
* **IV Abx** with **anaerobic cover** (cefuroxime. metronidazole)
39
Generate a management plan for gastrointestinal perforation- SURGICAL
**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
Identify possible complications of gastrointestinal perforation
Large and Small Bowel - **peritonitis**
Oesophagus - **mediastinitis**, shock, overwhelming sepsis and death
41
Summarise the prognosis for patients with gastrointestinal perforation
**_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
Define gastroenteritis
**Acute inflammation of the lining of the GI tract,** manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
43
What pathogens can cause gastroenteritis?
* **viruses**
* **bacteria**
* **protozoa**
* **toxins** contained in contaminated food or water (faecal-oral route)
44
State some organisms that are responsible for dyssentry
CHESS:
* **Campylobacter** jejuni
* Haemorrhagic **E Coli** O157
* **Entamoeba** histolytica
* **Salmonella**
* **Shigella**
45
What is a common cause of gastroenteritis in the elderly on Abx?
C. Difficile
46
State some commonly contaminated foods and the organisms responsible
* 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
Summarise the epidemiology of gastroenteritis
**COMMON**- 20% UK population/anum
Diarrhoeal disease remains a **leading cause of mortality worldwide.**
Most deaths are in young children in developing countries.
48
Recognise the presenting symptoms of gastroenteritis
**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
How does the onset of symptoms give an indication of the cause of gastroenteritis?
**Toxins** = early (1-24 hours)
**Bacterial/viral/protozoal** = 12+ hour
50
Recognise the signs of gastroenteritis on physical examination
* **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
What is important to consider when a patient presents with gastroenteritis?
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
List some systemic symptoms and signs of dehydration on examination
_Symptoms:_
* **Thirst**
* **Decreased urine output**
* **Dry mucous membranes;** check tongue and mouth
* Altered **mental state;** drowsiness.
_On examination:_
* **SBP \<100** mmHg
* **HR \>90**bpm
* **Cold** peripheries
* **RR \>20**
* **NEWS \>5**
53
Identify appropriate investigations for gastroenteritis
**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
Generate a management plan for gastroenteritis
_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
What are the 3 key treatment goals for gastroenteritis?
* Prevent and treat **volume depletion**
* Maintain **nutrition**
* **Reduce transmission** of the virus to other people.
56
How would you treat gastroenteritis caused by botulinium toxin?
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
How would you treat gastroenteritis caused by C. Difficile?
* **Isolate**
* Oral **metronidazole** 10-14 days
* If refractory: vancomycin
58
Identify the possible complications of gastroenteritis
* **Dehydration**
* **Electrolyte imbalance**
* **Prerenal failure**
* Secondary **lactose intolerance** (particularly in infants)
* **Sepsis and shock**
59
Which pathogens can be responsible for:
* Guillan-Barre syndrome
* HUS
* Paralysis of respiratory muscles
* 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
Summarise the prognosis for patients with gastroenteritis
Good prognosis because most cases are self-limiting
61
