Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI AND SURGERY > DISORDERS OF THE STOMACH, DUODENUM AND OESOPHAGUS > Flashcards

DISORDERS OF THE STOMACH, DUODENUM AND OESOPHAGUS Flashcards

1
Q

What is the difference between gastritis and gastropathy?

A

Gastritis is inflammation associated with mucosal injury
Gastropathy is epithelial cell damage and regeneration without inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What classification tool is used for gastritis?

A

Sydney system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the most common causes of gastritis?

A

H.pylor is the most common
Autoimmune gatsritis in 5% of cases
Viruses
Duodenogastric reflux
Specific causes e.g. crohns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 types of gastritis?

A

Acute gastritis
Atrophic gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is acute gastritis?

A

Inflammation of gastric mucosa that comes on suddenly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is atrophic gastritis?

A

Chronic inflammation of the gastric mucosa that causes epithelial metaplasia, mucosal atrophy and gland loss
Can lead to gastric intestinal metaplasia which is a precursor to gastric cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is autoimmune gastritis?

A

A pangastritis (affects fungus and body) which leads to Atrophic gastritis and loss of parietal cells = achlorhydria and intrinsic factor deficiency = pernicious anaemia symptoms
Metaplasia of intestinal cells is common
Serum autoantibodies to gastric parietal cells are common
Antibodies to intrinsic factor are rarer but more significant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are examples of viruses that can cause gastritis?

A

Cytomegalovirus
Herpes simplex virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes gastropathy?

A

Irritants e.g. drugs, NSAIDs, alcohol
Bile reflux
Chronic ingestion
Severe stress
Burns
Trauma
Shock
Renal failure
Portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of gastropathy can severe stress cause?

A

Stress ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of gastropathy can burns cause?

A

Curling ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are curling ulcers?

A

an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What type of gastropathy can portal hypertension cause?

A

Portal gastropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the signs and sympotms of gastritis?

A

May be asymptomatic
Epigastric pain
N+v
Mucosal ulcers
Haemorrhage, haematemesis, melena
IDA or pernicious anaemia - may cause symmetrical neuropathy in lower limbs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is gastritis/gastropathy diagnosed?

A

Endoscopic biopsy
H.pylori detection - serology, stool antigen test, urease breath test
Anti-IF or anti-parietal antibodies
Increased serum gastrin and decreased serum pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does gastritis cause an increase in serum gastrin?

A

Parietal cell loss causes achlorhydria which causes unrestricted gastrin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is gastritis or gastropathy managed?

A

Remove offending agents
Eradicate H.pylori with triple therapy
Correct vitamin deficiencies in autoimmune atrophic gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Whats the triple therapy to eradicated H.pylori?

A

PPI
Clarithromycin
Amoxicillin
- for 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which area of the stomach is most likely affected in
A) autoimmune atrophic gastritis
B) infectious atrophic gastritis

A

A- body and fungus (pangastritis)
B- antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is gastroparesis?

A

Delayed gastric emptying with no mechanical obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes Gastroparesis?

A

Most commonly idiopathic or secondary to poorly controlled diabetes
Iatrogenic - post-surgical or a medication side efefct

Others - amyloidosis, scleroderma, parkinsonism, MS, stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why can diabetes cause gastroparesis?

A

Neuropathy from hyperglycaemia can cause muscles to slow or not work at all (autonomic neuropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the symptoms and signs of Gastroparesis?

A

Chronic nausea and vomiting
Early satiety
Bloating
Abdominal pain upper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is gastroparesis diagnosed?

A

Endoscopy OGD to exclude mechanical obstruction (further imaging with CT or MRI may be needed)
Once this has been ruled out, diagnosis can be made with…
Gastric emptying scintigraphy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is scintigraphy?

A

a nuclear medicine scan that determines the rate of gastric emptying.
The patient must fast overnight before eating an isotope-labelled meal. The residual content of the stomach is then measured at 4 hours with more than 10% considered abnormal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What can help differentiate between myopathic and neuropathic causes of gastroparesis?

A

Gastroduodenal manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Gastroduodenal manometry?

A

a test of the pressure changes which occur within the stomach and upper intestine during digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are myopathic causes of gastroparesis?

A

Amyloidosis
Scleroderma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is gastroparesis managed?

A

Relief of symptoms
Correction of nutritional deficincies
Medical treatment - pro-motility agents
Surgery - gastric pacemaker insertion
Diet of frequent, small, low-fibre meals may help
Better glycaemic control in diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is dyspepsia?

A

a number of upper abdominal symptoms e.g. heartburn, acidity, pain or discomfort, nausea, wind, fullness or belching
Typically present for 4 weeks or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are features of dyspepsia that are suggestive of serious diseases?

A

Dysphagia
Weight loss
Vomiting
Anorexia
Haematemesis or melaena

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is GORD?

A

Gastro-oesophageal reflux disease (GORD) may be defined as symptoms of oesophagitis secondary to refluxed gastric contents through the lower oesophageal sphincter and irritates the lining of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Ulcers on other cards

A

X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is uninvestigated dyspepsia?

A

Symptoms in people who have not had an endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the causes of dyspepsia?

A

GORD
PUD
Functional dyspepsia
Barrett’s oesophagus
Upper GI malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is GORD/

A

Gastro-oesophageal reflux disease (GORD) is usually a chronic condition where there is reflux of gastric contents back into the oesophagus, causing predominant symptoms of heartburn and acid regurgitation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is proven GORD?

A

refers to endoscopically-determined reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What can cause GORD?

A

Oesophagitis
Endoscopy-negative reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is Endoscopy-negative reflux disease?

A

when a person has symptoms of GORD but endoscopy is normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the risk factors for developing GORD?

A

Lifestyle factors, such as obesity, trigger foods, smoking, alcohol, coffee, and stress.
Drugs that decrease the lower oesophageal sphincter pressure, such as calcium-channel blockers, anticholinergics, theophylline, benzodiazepines, and nitrates.
Pregnancy.
Hiatus hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Whats the annual and lifestyle risk of recurrence of untreated GORD symptoms?

A

Annual risk is 50%
Lifetime risk is 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What can GORD predispose people to?

A

10-15% will develop Barretts oesophagus and 1-10% of these will develop oesophageal adenocarcinoma over the next 10-20 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How should GORD be managed?

A

Advice on lifestyle measures and sleeping with the head of the bed raised.
Reviewing and stopping any drugs that may be exacerbating symptoms, if possible and appropriate.
Offering a full-dose PPI for 4 weeks for proven GORD, to aid healing.
Offering a full-dose PPI for 8 weeks for proven severe oesophagitis, to aid healing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is functional dyspepsia?

A

people with dyspepsia symptoms and normal findings on endoscopy
Most common diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the 2 subtypes of functional dyspepsia?

A

Epigastric pain syndrome, where intermittent or burning pain is localized to the epigastrium.
Post-prandial distress syndrome, where there is post-prandial fullness or early satiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is functional dyspepsia managed?

A

Offering advice on lifestyle measures that may improve symptoms.
Assessing for stress, anxiety, and depression, and managing these appropriately. (Considered a gut:brain interaction)
Reviewing and stopping any drugs which may be exacerbating symptoms, if possible and appropriate.
Always test for H.pylori if status is mot known

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

When should you refer a person with suspected oesophageal cancer for urgent endoscopy?

A

With dysphagia or
Aged 55 and over with wright loss and upper abdo pain or reflux or dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

When should you refer a person with suspected oesophageal cancer for non-urgent endoscopy?

A

For those who have haematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

When should you refer a person with suspected stomach cancer for urgent endoscopy?

A

Upper abdominal mass consistent with stomach cancer
People with dysphagia
Those aged 55 and over with upper abdominal pain, reflux or dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When should you refer a person with suspected stomach cancer for non-urgent endoscopy?

A

People with haematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How should you assess someone with dyspepsia?

A

Ask about any alarm symptoms thta may suggest serious underlying pathology
Assess frequency, duration and pattern of sympotms
Ask about FHx of upper GI maliganncy
Lifestyle factors that may cause symptoms e.g. obesity, trigger foods, smoking, alcohol
Assess for stress, anxiety and depression which may worsen symptoms
Review meds
Examine for weight loss, signs of anaemia, abdominal masses and tenderness
Consider FBC to check for anaemia and raised platelet count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What foods can worsen dyspepsia?

A

coffee, chocolate, tomatoes, fatty or spicy foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What drugs can cause or exacerbate dyspepsia?

A

alpha-blockers
anticholinergics
aspirin
benzodiazepines
beta-blockers
bisphosphonates
calcium-channel blockers
corticosteroids
nitrates
NSAIDs
theophyllines
TCAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How should you manage dyspepsia with an unidentified cause?

A

Advice on lifestyle measures e.g. losing weight, avoiding trigger foods, eating smaller meals, stop smoking, reduce alcohol
Stop any meds that may be causing it
Offer either a PPI for 1 month or test for H.pylori. If symptms persist then switch to alternative strategy
Advise on follow up appointments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How should endoscopically proven oesophagitis be treated?

A

Full dose PPI for 1-2 months

(If refractory then low dose treatment as required and if no response then double-dose PPI for 1 month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How should endoscopically negative reflux disease be managed?

A

Full dose PPI for a month

(If no response then low dose treatment as required and if no response then H2RA or pro kinetic for 1 month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are complications of GORD?

A

Oesophagitis
Ulcers
Anaemia
Benign strictures
Barretts oesophagus
Oesophageal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Why is the oesophagus more sensitive to the effects of stomach acid in comparison to the stomach?

A

The oesophagus has a squamous epithelial lining whilst the stomach has columnar epithelial lining so its more protected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Whats an alternative to PPIs for managing GORD?

A

Ranitidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is ranitidine and wats its moa?

A

A H2 receptor antagonist

The reversible inhibition of H2-receptors in gastric parietal cells results in a reduction in both gastric acid volume and concentration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What surgery can be done for GORD?

A

Laparoscopic Fundoplication - tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is Barrett’s oesophagus?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is Barrett’s oesophagus?

A

When constant acid reflux results in metaplasia on the lower oesogeal epithelium causing a change from squamous to columnar epitheiulim - will cause an improvement in their reflux symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Whats the complication of Barrett’s oesophagus?

A

It’s a pre malignant condition and is a risk factor for the development of adenocarcinoma of the oesophagus - 3-5% lifetime risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What monitoring is done for Barrett’s oesophagus?

A

For patients with metaplasia - Monitored for adenocarcinoma of the oesophagus by regular endoscopy every 3-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Outline the steps in progression from Barrett’s oesophagus to oesophageal adenocarcinoma?

A

No dysplasia
Low grade dysplasia
High grade dysplasia
Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is Barrett’s oesophagus managed?

A

PPI
Regular aspirin can reduce the rate of adenocarcinoma developing
Ablation treatment during endoscopy to replace columnar epitelium with squamous cell epithelium - done for patients with dysplasia of any grade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the subdivisions of Barrett’s oesophagus?

A

short <3cm
Long >3cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Outline the histological features of Barrett’s oesophagus?

A

Columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

70
Q

What are the risk factors for Barrett’s oesophagus?

A

GORD - strongest risk factor
Male gender 7:1
Smoking
Central obesity

(Interestingly not alcohol although it’s associated with GORD and oesophageal cancer)

71
Q

What is cyclical vomiting syndrome?

A

characterized by typical bouts of intense vomiting lasting for hours to days, separated by periods with no symptoms. It can occur in children or adults.

72
Q

What is cyclical vomiitng syndrome linked to?

A

Migraine headaches - cause not known

73
Q

What are some known triggers for cyclical vomiting syndrome?

A

Frequent cannabis use - cannabinoid hyperemesis syndrome
Emotional or physical stress
Food and drinks - chocolate cheese caffeine alcohol MSG
Extremes of temperature
Menstrual cycle
Allergies

74
Q

Outline the stages of cyclical vomiting syndrome?

A

Prodromal phase - feel an episode of vomiting is about to start, intense sweating and nausea for a few mins-hours, appear unusually pale

Vomiting phase - vomit up to 6 times an hour for up to 10 days, abdo pain, unable to talk/move. May have other symptoms e.g. temperature, diarrhoea, headache

Recovery phase - vomiting, retching and nausea stops and other symptoms improve. Recovery can take a few hours-days

Well phase - no symptoms

The cycle is usually regular and predictable, with the same symptoms starting at the same time of the day or night and lasting for the same length of time.

75
Q

Who’s affected by cyclical vomiting syndrome?

A

More common in children, starting between 3 and 7
Can affect adults
Those with PMHx or FHx of migraines more likely
Children may stop getting symptoms as they got older or may continue. They may have migraines as an adult

76
Q

How is cyclical vomiting syndrome managed?

A

Antiemetics
IV rehydration and electrolyte replacement during bouts
Avoidance of any known treatments
Prophylactic treatment of migraine

77
Q

Outline the 3 pathological causes for gastroparesis?

A

The pylorus/duodenum may be obstructed by an ulcer/tumor, or by something large and indigestible that was swallowed.
The pyloric sphincter at the exit of the stomach may not open enough or at the right times to allow food to pass through - neurological damage
The normally rhythmic, 3 per minute contractions of the lower part of the stomach can become disorganized so that the contents of the stomach are not pushed towards the pyloric sphincter. This also usually has a neurological basis; the most common known cause is longstanding diabetes mellitus, but in many patients the cause of delayed gastric emptying is unknown, so the diagnosis given is idiopathic gastroparesis.

78
Q

What is dumping syndrome?

A

Rapid gastric emptying - when the jejunum fills too quickly with undirected food from the stomach

79
Q

What is early dumping vs late dumping?

A

“Early” dumping begins during or right after a meal. “Late” dumping happens 1 to 3 hours after eating.

80
Q

Which 2 central areas are responsible for triggering nausea and vomiitng?

A

Nucleus tractus solitarius in the medulla - acts as a central pattern generator for vomiting
Area postrema in the floor of the fourth ventricle and contains the chemoreceptor trigger zone

81
Q

What are the 5 receptors in the CTZ?

A

5-HT receptors
• histamine H1 receptors
• muscarinic receptors
• dopamine D2 receptors
• substance P (neurokinin-1-neuropeptide).

82
Q

What substances can stimulate the CTZ directly as they are carried through the blood stream?

A

Opioids
Hormones
Ketoacidosis
Urea

83
Q

What are the 2 ways in which stimulants can cause vomiting?

A

Centrally or directly in the bowel

84
Q

Where is the chemoreceptor trigger zone?

A

In the area postrema in the medulla oblongata - on the floor of the fourth ventricle

85
Q

Is the CTZ in or outside the blood-brain barrier?

A

Outside - more permeable to circulating substances e.g. cytotoxic chemotherapy

86
Q

What are the sources of input to the vomiting centre?

A

CTZ
Vestibular system e.g. motion sickness
Vagus nerve
Vagal and enteric nervous system - GI mucosa irritation

87
Q

What receptors does the CTZ have?

A

D2
5-HT3
Opioid
ACh
Substance P receptors

88
Q

Outline how the vestibular system can be a source of input to the vomiting centre?

A

Vestibular system in labyrinth in inner ear sends information via vestibvulocochlear nerve. This gets sent to the vestibular nuclei in the pons and then to the CTZ which will then send signals to the vomiting centre = trigger emesis
plays a major role in motion sickness

89
Q

Which receptors are found in the vestibular nuclei?

A

Histamine 1 receptors
Muscarinic receptors

90
Q

Which receptors are found in the vomiting centre?

A

Muscarinic receptors

91
Q

Outline how the higher brain centre can be a cause of vomiting

A

Severe emotion, pain, smells or sights -> higher brain centres stimulated -> vomiting centre stimulated -> vomiting reflex

92
Q

Outline how the emetic reflex can be stimulated in the GIT?

A

In the stomach, enterochromaffin cells release serotonin in response to cytotoxic agents/infection etc -> stimulates 5HT3 receptors on sensory nerve fibres of Vagal nerve > vomiting centre stimulated

93
Q

Outline the epidemiology of gastric cancer?

A

4th most common cancer worldwide
2nd leading cause of cancer-related mortality
Peak incidence 50-70. Rare under 30
Highest incidence in Eastern Asia, Eastern Europe and South America
M:w 2:1

94
Q

How is the incidence of gastric cancer changing and why?

A

Worldwide its falling probably due to reductions in H.pylori and improvements in food storage
Incidence of proximal gastric cancer is increasing in the west

95
Q

Whats the most prevalent gastric cancer which is seen in >90% of cases?

A

Adenocarcinoma

96
Q

What are the aetiological factors of gastric cancer?

A

H.pylori strongly linked to distal gastric cancers - responsible for 60-70% of cases
Dietary factors - high salt, nitrates, nitrosamines. Fresh fruit and veg particularly those containing vitamin C and A are known to have a beneficial effect
Tobacco smoking
Genetic abnormalities
Fhx first degree relative 2-3 fold increase
Pernicious anaemia due to accompanying atrophic gastritis
Partial gastrectomy - maybe due to untreated H.pylori?

97
Q

How do we determine if its an oesophageal or a gastric cancer?

A

If the epicentre of the tumour is </= 2cm from the GOJ then it’s oesophageal cancer
If the epicentre of the tumour is >2cm from the GOJ then its a gastric cancer

98
Q

How are gastric cancers classified histologically?

A

Described by Lauren criteria 1965 into 2 histological subtypes
Intestinal type - well differentiated and represent intestinal epithelium. Better prognosis. Older people. Associated with H.pylori infection so most tumours in high income countries
Diffuse - arise from normal gastric mucosa. Affects younger people. Worse prognosis. Affects LIC

99
Q

What are the main difference between intestinal and diffuse gastric cancer

A

Intestinal is more commonly seen in males, older ages and has a better prognosis. Strong envionrmental association. Tend to affect distal stomach
Diffuse has an equal sex prevalence, seen in younger patients and a worse prognosis. Undifferentiate. May affect any part of the stomach. Key event is loss of expression of E-cadherin

100
Q

What is linitis plastica?

A

Aka leather bottle stomach
It’s when diffuse gastric cancer involves a major portion, or all of the stomach

the term is also used to describe the condition of a rigid, non-distensible stomach

101
Q

What are early and advanced gastric cancer?

A

Early: cancer confined to the mucosa or submucosa. Regardless of the presence of lymph node metastasis. Much better prognosis (>90% five-year survival).

Advanced: cancer invades the muscularis and beyond. Much worse prognosis with five year survival ≤60%. May be associated with lymph node and distant metastasis.

102
Q

Whats the most common genetic factor in the aetiology of gastric cancer?

A

Loss of tumour suppressor gene p53 - occur sin 70%

103
Q

Can ulcers develop into cancer?

A

No
Benign ulcers cannot develop into malignant ulcers or cancers
Some cancers can cause malignant ulcers

104
Q

What is hereditary diffuse gastric cancer?

A

a rare inherited genetic condition associated with an increased risk of gastric cancer.
Associated with CDH1 gene
Autosomal dominant pattern
Average age diagnosed is 38
Also increases the risk of lobular breast cancer
Associated with cleft lip or cleft palate also
Recommended prophylactic total gastrectomy due to high risk of cancer

105
Q

What is the Correa cascade?

A

The classic sequence of histolgical lesions for intestinal type adenocarcinoma (most common gastric cancer)

Normal gastric mucosa -> chronic non-atrophic gastritis -> chronic atrophic gastritis -> intestinal metaplasia -> dysplasia

106
Q

How does gastric cancer present?

A

Epigastric pain which is relived by food and antacids
Fever
Anorexia
Lethargy
Weight loss
Dysphagia if gastric cardia involved
Indigestion and dyspepsia
Nausea and vomiting - can be severe if tumour encroaches on pylorus
Haematemesis and maleaba
Post-prandial fullness
Palpable epigastric mass with abdominal tenderness
Dermatomyositis and Acanthosis nigricans

If distant spread.. may cause pallor, cachexia, Virchow node lymphadenathy, hepatomegaly if mets in lover and Sister Mary Joseph nodule if periumbilical metastasis, ascites or jaundice if liver metss

107
Q

Where does gastric cancer commonly spread to?

A

Liver
Lymph nodes
Peritoneum
Bones
Brain
Lungs

108
Q

When does a pt need an urgent 2WW referral for suspected gastric cancer?

A

Upper abdominal mass consistent with gastric cancer OR
Dysphagia OR
>55 years with weight loss and either upper abdominal pain, reflux or dyspepsia

109
Q

What proportion of those presenting with gastric cancer will have metastasis?

A

1/3rd (often diagnosed late)

110
Q

When should you do a non-urgent referral for gastric cancer?

A

Haematemesis, OR
> 55 years with treatment resistant dyspepsia, OR
> 55 years with upper abdominal pain and anaemia, OR
Thrombocytosis with one of the following: Nausea/vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
Nausea/vomiting with one of the following: weight loss, reflux, dyspepsia
Upper abdominal pain

111
Q

What are the types of gastric cancerS?

A

Adenocarcinoma
Gastrointestinal stromal tumours
Carcinoid tumours
Primary gastric lymphoma

112
Q

How is gastric cancer investigated?

A

Bloods - FBC, serum iron/transferring/TIBC, U&E, LFTs, bone profile, clotting screen, renal function
CT chest/abdo/pelvis
PET-CT for pt with potentially resectable disease
Gastroscopy and biopsies for histological assessment. Can also carry out an endoscopic ultrasound at the time time
Diagnostic laparoscopy
HER2 testing

113
Q

What is imaging important when investigating gastric cancer?

A

Helps stage the camera has it looks for distant spread

114
Q

Why should gastric cancer pt with potentially resectable disease have a PET-CT?

A

to assess for distant disease not detected by conventional CT.

115
Q

Why should HER2 testing be completed on pt with metastatic gastric cancer?

A

Gastric cancers can be HER2 positive in up to 30% of cases and management can be targeted to this protein

116
Q

What staging is done for gastric cancer?

A

TNM staging

117
Q

Outline TNM staging for gastric cancer?

A

TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
Tis: Carcinoma in situ: intraepithelial tumour without invasion of the lamina propria
T1: Tumour invades lamina propria or submucosa
T1a: Tumour invades the lamina propria or the muscularis mucosae
T1b: Tumour invades the submucosa
T2: Tumour invades the muscularis propria
T3: Tumour penetrates the subserosal connective tissue without invasion of the visceral peritoneum or adjacent structures
T4: Tumour invades the serosa or adjacent structures
T4a: Tumour invades the serosa
T4b: Tumour invades adjacent structures

Node
NX: Regional lymph node(s) cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis in 1–2 regional lymph nodes
N2: Metastasis in 3–6 regional lymph nodes
N3: Metastasis in 7 or more regional lymph nodes

Metastasis
MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis or positive peritoneal cytology

118
Q

What is a signet ring cell?

A

a signet ring cell is a cell with a large vacuole. The malignant type is seen predominantly in carcinomas. Signet ring cells are most frequently associated with stomach cancer, but can arise from any number of tissues including the prostate, bladder, gallbladder, breast, colon, ovarian stroma and testis.

119
Q

With gastric cancer… at presentation, what proportion of pt are at stage 3 or 4?

A

2/3rds

120
Q

Whats the 5 year survival rate at stage 1 gastric cancer?

A

88%

121
Q

Whats the 5 year survival rate at stage 4 gastric cancer?

A

5%

122
Q

How is gastric cancer managed?

A

Early non-ulcerated mucosal lesions can be removed endoscopically by either endoscopic mucosal resection or endoscopic submucosal dissection.
If the pt is an operative candidate then surgery is the most effective form of treatment
Chemotherapy

Other options - radiotherapy, monoclonal antibodies against HER2, palliative care

123
Q

Which gastric cancers are considered operable?

A

Pt with T1 tumours without lymph node involvement or metastasis
Pt stage 1B-3 may be considered if fit enough. This will have to be in combination with chemo or chemoradiotherapy

Not suitable - evidence of distance spread

124
Q

What type of surgery can be offered for gastric cancer?

A

Subtotal gastrectomy
Total gastrectomy
Oesophageal-gastrectomy if GOJ involvement

125
Q

What is the principle anti-cancer therapy in gastric cancer?

A

Chemotherapy

126
Q

What chemotherapy is given for gastric cancer?

A

Chemotherapy combination regimens depend on whether the tumour is HER2 positive.
HER2-negative advanced/metastatic gastric cancer: double/triple chemotherapy regimens (e.g. oxaliplatin, 5-Fluorouracil +/- epirubicin)
HER-2-positive advanced metastatic gastric cancer: Trastuzumab (monoclonal antibody against HER2-receptor) in combination with platinum/fluoropyrimidine chemotherapy.

127
Q

What are gastrointestinal stromal tumours?

A

A subset of gastrointestinal mesenchymal tumours of varying differentiation
They are of stromal origin

128
Q

Which mutations are associated with gastric stromal tumours?

A

Mutations occur in cellular protocol-oncogene KIT which leads to activation and cell-surface expression of the tyrosine kinase KIT and also in platelet-derived growth factor receptor-alpha in some pt

129
Q

Who do gastrointestinal stromal tumours affect?

A

55-65 year olds

130
Q

Whats the pathophysiology of diffuse type gastric adenocarcinoma?

A

Lack of adhesion molecule E-cadherin
Genetic mutation of CDH1 gene -> inactivation of CDH1 -> non-functional E-cadherin

131
Q

Whats the pathophysiology of intestinal type gastric adenocarcinoma?

A

Due to environmental factors

132
Q

How are gastrointestinal stroma tumours treated?

A

Surgery
Imatinib a tyrosine kinase inhibitor may be used for unresectable or metastatic disease, or even as adjunctive therapy

133
Q

What is primary gastric lymphoma?

A

The most common extranodal non-hodgkin lymphoma
Accounts for <15% of gastric malignancies and 2% of lymphomas
90% are MALT or diffuse large-B cell lymphoma of the stomach

134
Q

Whats the cause of primary gastric lymphoma?

A

About 90% of cases are due to H.pylori infection
Chromosome abnormalities have also been noted

135
Q

How is primary gastric lymphoma managed?

A

Eradication of H.pylori infection - 50% will show resolution at 3 months
Stage 3 or 4 disease is treated with surgery or chemotherapy

136
Q

Whats the prognosis of primary gastric lymphoma?

A

90% 5 year survival

137
Q

What are carcinoid tumours?

A

Neuroendocrine tumours

138
Q

How prevalent are gastric polyps?

A

Found in about 15 of endoscopies, usually by chance

139
Q

How do gastric polyps present?

A

Rarely produce symptoms but larger lesions can result in anaemia or haematemesis

140
Q

Whats the most common type of gastric polyp?

A

Hyperplastic polyp

141
Q

What are the types of gastric polyp?

A

Hyperplastic polyps 75%
Adenomatous polyps 5%
Cystic gland polyps
Inflammatory fibroid polyps <0.1%

142
Q

What are Hyperplastic polyps?

A

Hyperplastic polyps result from hyper-regenerative epithelium in response to an underlying chronic inflammatory stimulus. They are therefore observed in the setting of chronic inflammatory conditions (eg, chronic atrophic gastritis), H. pylori, pernicious anemia, adjacent to ulcers and erosions, and at sites of gastroenterostomies

They are generally benign, but have some malignant potential. Hyperplastic polyps >0.5 cm should be resected completely.

143
Q

What are adenomatous polyps?

A

usually solitary lesions in the antrum. Approximately 3% progress to gastric cancer, especially if greater than 2 cm in diameter, but they are not a common cause of gastric cancer (compare this with colorectal cancer).

144
Q

What are cystic gland polyps?

A

contain microcysts that are lined by fundic-type parietal and chief cells. They are located in the fundus and body of the stomach. They are found in otherwise normal subjects, but are especially common in familial polyposis syndromes and patients on PPIs.
Their malignant potential is negligible

145
Q

What are inflammatory fibroid polyps?

A

benign spindle cell tumours infiltrated by eosinophils.
Arise within the submucosa of the GIT
Excision of these polyps is indicated because of their propensity to enlarge and cause obstruction.
Extremely rare

146
Q

What is a duodenal haematoma?

A

results in haematoma formation in the duodenal wall. It may occur as a result of blunt abdominal trauma, non-accidental injury to children and spontaneously in anti-coagulated patients.

147
Q

What is Brunner’s gland hyperplasia?

A

Brunner’s gland hyperplasia makes up 10.6% of benign tumors in the duodenum and rarely presents any symptoms

148
Q

What is achalasia?

A

Loss of coordination of oesophageal peristalsis and relaxation of the lower oesophageal sphincter
Causes LOS to contract and oesophagus above to be dilated
This prevents the passage of food and liquids into the stomach

149
Q

What causes achalasia?

A

Degenerative loss of ganglia from Auerbach’s plexus
In some people its linked to a viral infection or autoimmune conditions

150
Q

When does achalasia typically present?

A

Middle age
Equally common in men and women

151
Q

What are the clinical features of achalasia?

A

dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients

152
Q

What investigations are done for achalasia?

A

oesophageal manometry- excessive LOS tone which doesn’t relax on swallowing (considered the most important diagnostic test)
barium swallow - shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray - wide mediastinum + fluid level

153
Q

How is achalasia treated?

A

Pneumatic dilation - preferred first-line option
Surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
Intra-sphincteric injection of botulinum toxin may be used if high surgical risk

154
Q

What is seen on barium swallow in oesophageal carcinoma?

A

Apple-core sign - narrowed oesophagus appearing similar to the core of an apple

155
Q

How do oesophageal cancer and achalasia present differently?

A

Oesophageal cancer typically has dysphagia of food as first presentation followed by dysphagia for liquids
Achalasia presents with dysphagia for solids and liquids at the same time

156
Q

What is seen on a barium swallow in achalasia?

A

narrowing of the distal oesophagus with subsequent dilatation of the proximal oesophagus (bird beak sign)

157
Q

What is Plummer-Vinson syndrome?

A

a triad of iron deficiency anaemia, atrophic glossitis and oesophageal webs or strictures.

158
Q

What is associated with HNPCC?

A

Pancreatic cancer
Endometrial cancer

159
Q

Whats the management for life threatening C.diff infection?

A

Oral vancomycin and IV metronidazole

160
Q

What will iron studies show in haemachromatosis?

A

High transferrin saturation
High ferritin
Low TIBC
(If haemachromatosis is the diagnosis to be, expect a low TIBC.Plus transferrin and ferritin oh so high, give venesection and chelation to say goodbye)

161
Q

What are common complications of trans jugular intrahepatic portosystemic shunt?

A

Exacerbation of hepatic encephalopathy - most common!!
Acute liver failure
Biliary injury
Thrombosis

162
Q

Whats the first line pharmacological treatment for constipation in patients with IBS?

A

Ispaghula husk or other bulk forming laxatives

163
Q

How does omeprazole and esomeprazole affect efficacy of clopidogrel?

A

They inhibit CYP2C19 which is needed to convert clopidogrel into it’s active metabolite = decreases its efficacy

164
Q

Why is metoclopramide suggested as the best anti-emetic to use with migraines?

A

Because its a pro kinetic so it helps relieve the gastric stasis that slows the transit/absorption of drugs during an acute migraine arrack
It’s even suggested that it should be considered even in the absence of nausea and vomiting, due to its pro kinetic effects

165
Q

Why should metoclopramide not be taken for longer than 5 days in a treatment course?

A

Due to the risk of EPS with long term use

166
Q

How is diagnosis of spontaneous bacterial peritonitis done?

A

Paracentesis - confirmed by a neutrophil count >250 cells/ul

167
Q

What is another name for pharyngeal pouch?

A

Zenker’s diverticulum

168
Q

What is pharyngeal pouch?

A

posteromedial diverticulum through Killian’s dehiscence (a triangular area in the wall of the pharynx between thyropharyngeus and cricopharyngeus muscles)

169
Q

Who is likely to get pharyngeal pouch?

A

Older pt
Men are 5x more likely to get it

170
Q

What are the features of pharyngeal pouch?

A

dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis

171
Q

How do we investigate pharyngeal pouch?

A

barium swallow combined with dynamic video fluoroscopy

172
Q

How do we manage pharyngeal pouch?

A

surgical myotomy and resection

GI AND SURGERY (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions