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Y1 GI > GORD/Dyspepsia/PUD/Upper GI Bleeding > Flashcards

GORD/Dyspepsia/PUD/Upper GI Bleeding Flashcards

1
Q

What are the causes of GORD

A

1) incompetent LOS
2) Poor oesophageal clearance
3) Visceral sensitivity

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2
Q

What causes relaxation of LOS

A

Parasympathetic activity - release ACh and substance P

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3
Q

What are the symptoms of GORD

A 
Heartburn 
Regurgitation
Dysphagia
Odynophagia 
cough
Hoarse voice
dyspepsia
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4
Q

What are the red flag symptoms

A 
dysphagia 
weight loss
haematemesis 
malena 
anaemia 
persistent vomiting
Palpable mass
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5
Q

What are the symptoms for dyspepsia

A

Epigastric pain
postprandial fullness (bloating / belching)
early satiety

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6
Q

What are the risk factors for GORD

A 
Smoking
Alcohol
Obesity
Family history of GORD
pregnancy 
NSAID
Caffeine
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7
Q

What exacerbates heart burn

A

After meals

Worse when lying down or bending forward

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8
Q

What is odynophagia

A

Painful swallowing

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9
Q

What are the complications for GORD

A 
Chronic oesophagitis (reflux oesophagitis) 
Barrett's oesophagus 
Oesophageal malignancy 
Reflex stricture
Reflux dental erosions 
Reflux laryngitis syndrome
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10
Q

Why should chronic oesophagitis be detected early

A

Because it is reversible
If not treated early, it can develop into Barrett’s oesophagus which is non-reversible and increases risk for oesophageal malignancy

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11
Q

Diagnosis of GORD

A

pH studies
Oesophageal manometry
Gastroscopy

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12
Q

Who is gastroscopy reserved for in GORD

A

For those patients with red flag symptoms/ considered for surgery/ sympatomatic despite treatment

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13
Q

What is the management for GORD (first line)

A

Lifestyle management + full dose PPI

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14
Q

What are the lifestyle advices given to patients with GORD

A 
avoid eating 2 hours before sleeping 
smoking cessation
decrease alcohol consumption 
elevate level of head when lying down 
weight loss if obese
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15
Q

What type of foods should be avoided in patients with GORD

A

spicy / sour / caffeine

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16
Q

When is H2 receptor antagonist used in GORD

A

If the patient does not respond to PPI

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17
Q

What is the full dose of omeprazole

A

40mg once a day

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18
Q

Name of surgery given to GORD patients

A

Nissen fundoplication

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19
Q

When is surgery for GORD indicated

A

When the patient doesn’t respond to drug treatment

When the patient responds to PPI but wish to solve GORD at once

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20
Q

What are the foregut structures

A 
Oesophagus 
stomach
liver
gall bladder
pancreas 
spleen
first half of duodenum
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21
Q

What are the 2 causes of dyspepsia

A

Organic causes - use of NSAID / peptic ulcer disease / gastric cancer
Functional dyspepsia - idiopathic

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22
Q

What is dyspepsia

A

A term used to describe upper GI tract symptoms

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23
Q

How long does dyspepsia usually occur

A

4 or more weeks

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24
Q

What should you do if a patient with dyspepsia present with other red flag symptoms

A

Refer them to specialists (suspect malignancy)

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25
Q

Management of patients with dyspepsia without red flag symptoms

A

Lifestyle management + antacids

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26
Q

What is the next step management if patients still experience dyspepsia after initial treatment

A

Suspect H. pylori -> test for H.pylori
If positive -> antibiotics + PPI
If negative -> if more than 55 years old -> referral
If negative -> if less than 55 years old -> PPI (treat as functional dyspepsia)

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27
Q

What medication should be stopped before H. pylori testing

A

Proton Pump inhibitors

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28
Q

What are the drugs used against H. Pylori

A

amoxicillin + clarithromycin + PPI (triple therapy)

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29
Q

What drugs are used against H. pylori if the patient is penicillin allergic

A

metronidazole + clarithromycin + PPI

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30
Q

What may severe GORD cause

A

aspiration pneumonia

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31
Q

What is Barett’s oesophagus

A

When the oesophageal mucosa undergoes metaplastic change from stratified squamous cells to simple columnar cells

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32
Q

What are the types of oesophagitis

A

Acute oesophagitis
Chronic oesophagitis (reflux oesophagitis)
Allergic oesophagitis

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33
Q

Which type of oesophagitis is rare

A

Acute oesophagitis

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34
Q

Which group of people is susceptible to infective acute oesophagitis (AO due to infection)

A

Immunocompromised individuals

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35
Q

What infections can cause acute oesophagitis

A

Herpes
CMV
candidiasis

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36
Q

Cause of reflux oesophagitis

A

Inflammation due to reflux of low pH gastric content

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37
Q

What are the changes in mucosa for reflex oesophagitis

A

basal hyperplasia and lengthening of papilla

Increase in intraepithelial neutrophils, lymphocytes and eosinophils

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38
Q

What causes basal hyperplasia in reflux oesophagitis

A

low grade inflammation causes an increase in cell desquamation -> increase in proliferation to compensate

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39
Q

What are the complications of reflux oesophagitis

A

ulceration
stricture
Barrett’s oesophagus

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40
Q

Timeline of chronic oesophagitis

A

Reflux oesophagitis -> Barrett’s oesophagus (metaplasia) -> low grade dysplasia -> high grade dysplasia

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41
Q

What does Barrett’s oesophagus increase the risk for

A

Oesophageal adenocarcinoma, carcinoma

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42
Q

What are the treatments for low grade dysplasia (Barrett’s)

A

PPI + endoscopy surveillance every 6 months

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43
Q

What are the treatments for high grade dysplasia (Barrett’s)

A

Endoscopic resection - radiofrequency ablation / endoscopic mucosal resection / endoscopic submucosal resection

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44
Q

Features of allergic oesophagitis

A

Large numbers of eosinophils

Not due to acid reflux

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45
Q

Risk factors for allergic oesophagitis

A

Family history of allergies
asthma
male
common in young people

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46
Q

What is the treatment for allergic oesophagitis

A

Steroids

Montelukast

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47
Q

Types of oesophageal cancer

A

Adenocarcinoma

Squamous cell carcinoma

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48
Q

2 types of gastric adenocarcinoma

A

Intestinal

DIffuse

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49
Q

Where is the most common site of oesophageal cancer

A

lower end of oesophagus

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50
Q

Which oesophageal cancer is Barrett’s oesophagus most associated to

A

Adenocarcinoma

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51
Q

Risk factors for oesophageal adenocarcinoma

A 
Barrett's oesophagus 
GORD
obesity
smoking 
age 
male
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52
Q

Risk factors for oesophageal squamous cell carcinoma

A 
Oeosphagitis 
Hot drinks 
Low intake of fibres and fruits
age
smoking 
alcohol 
GORD
Achalasia
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53
Q

Symptoms of oesophageal cancer

A 
Progressive dysphagia  
Heart burn 
Vomiting / regurgitation
haematemasis  
Weight loss
Anorexia 
Hoarse voice
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54
Q

How do oesophageal tumours invade other structures

A

Direct local invasion - e.g. to trachea
Through blood
Lymph nodes

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55
Q

Diagnosis of oesophageal cancer

A

endoscopy and take biopsy
CT scan to stage the cancer
PET scan to check for metastases

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56
Q

Management of oesophageal cancer

A

If early (Barrett’s, high grade dysplasia) - endoscopic resection
If intermediate (no local invasion / distant metastases / lymph nodes)
- chemotherapy + surgery
- neoadjuvant chemoradiotherapy + surgery

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57
Q

What is the surgery for oesophageal cancer called

A

Oesophagectomy

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58
Q

Types of gastritis

A

Acute gastritis

Chronic gastritis

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59
Q

Causes of chronic gastritis

A

Bacterial
Chemical
Autoimmune

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60
Q

Which pathogen is the most common cause of bacterial gastritis

A

H. pylori

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61
Q

How does H. pylori cause chronic gastritis

A

Induces release of IL-8 , causing inflammatory response and chronic inflammation if not cleared

62
Q

What is IL-8

A

A pro-inflammatory cytokine

63
Q

What type of bacteria is H.pylori

A

Gram negative

Spiral shaped bacilli

64
Q

Transmission of H. pylori

A

Oral to oral

Faecal to oral

65
Q

When do people usually become infected with H. pylori

A

As a child / young adulthood

66
Q

What conditions does chronic gastritis increase the risk for

A

Peptic ulcer disease
gastric adenocarcinoma
gastric lymphoma

67
Q

What causes chemical chronic gastritis

A

NSAID
Alcohol
Bile reflux

68
Q

What causes autoimmune gastritis

A

Presence of anti-parietal and anti-intrinsic factors antibodies

69
Q

What are intrinsic factors for

A

for absorption of vitamin B12

70
Q

What are the signs of vitamin B12 deficiency

A

Macrocytic (abnormally large RBC)
Pernicious anaemia
SACDC

71
Q

What is SACDC

A

when myelin sheath starts to wear away

72
Q

Types of gastric cancer

A

adenocarcinoma

lymphoma

73
Q

Types of gastric adenocarcinoma

A

Intestinal

diffuse

74
Q

Features of intestinal gastric adenocarcinoma

A
  • better prognosis
  • accounts for most of the non-cardia tumours
  • increased level of HER2 protein
  • most associated with H. pylori infection
75
Q

Features of diffuse gastric adenocarcinoma

A
  • poorer prognosis
  • associated with genetic changes in CDH1 gene
  • more in young patients
76
Q

What are HER2 proteins

A

growth-promoting proteins; associated with breast cancer and gastric cancer

77
Q

Which cancer is CDH1 gene mutation also associated to

A

Lobular breast cancer

78
Q

Symptoms of gastric cancer

A 
weight loss
gastric reflux
vomiting +/- haematemesis 
dyspepsia 
malena
79
Q

How may H.pylori infection lead to gastric adenocarcinoma

A

H. pylori infection -> chronic gastritis -> intestinal metaplasia (glandular cells become intestinal cells) -> dysplasia

80
Q

Type of epithelium in duodenum

A

simple columnar cell with crypts of lieuberkuhn between villi

81
Q

Type of epithelium in stomach

A

simple columnar cells with gastric glands

82
Q

Type of epithelium in oesophagus

A

stratified squamous cells

83
Q

What causes gastric lymphoma

A

Due to H.pylori
Continuous inflammation induces an evolution into a clonal B cell proliferation -> low grade lymphoma -> high grade lymphoma

84
Q

What lymphoid tissue does gastric lymphoma affect

A

mucosa associated lymphoid tissue (MALT)

85
Q

Where is MALT found

A

Lamina propria (where the mucosal immunity is)

86
Q

Metastases of gastric cancer

A

Lymph nodes of greater omentum
through blood - to liver first
transcolaemic - to organs in peritoneal cavity , ovaries

87
Q

Can low grade gastric lymphoma disappear completely

A

Yes, if H. pylori is eradicated

88
Q

Management of early gastric cancer

A

Endoscopic resection - radiofrequency ablation / endoscopic mucosal resection / endoscopic submucosal resection

89
Q

Management of intermediate gastric cancer

A

Perioperative chemotherapy (FLOT regime) + surgery

90
Q

Management of late gastric cancer

A

Chemotherapy + targetted molecular therapy (e.g. targetting HER2)

91
Q

Types of peptic ulcer

A

Gastric ulcer

Duodenal ulcer

92
Q

4 parts of duodenum

A

Superior
Descending
Inferior
Ascending

93
Q

Where does duodenal ulcer usually occur

A

Superior part of duodenum

94
Q

Compare between gastric and duodenal ulcer

A 
Gastric 
- equal gender distribution
- incidence increases with age
Duodenal
- associated with H. pylori
- more common in males
- more common than gastric ulcer
95
Q

Causes of peptic ulcer

A

H. pylori

NSAID

96
Q

What conditions are H. pylori associated to

A

Chronic gastritis
Gastric intestinal adenocarcinoma
Gastric lymphoma
Peptic ulcer disease (esp. duodenal)

97
Q

How does H. pylori cause peptic ulcers

A

1) cause hypergastrinemia by increasing gastrin production and reducing somatostatin
2) damages mucous producing goblet cells and epithelial cells
3) this causes an increase in gastric acid secretion and decrease in protective mucous
4) allows H. pylori to enter stomach lining and damage deeper layers
5) acid enters, causing ulcer

98
Q

Which cell produces gastrin

A

G cells

99
Q

When is gastrin normally released

A

In response to distention of stomach
presence of amino acids / peptides
increase in pH

100
Q

Does everyone with H. pylori infection develop into peptic ulcer

A

No, only 20-40%

101
Q

How does NSAID cause peptic ulcers

A

NSAID inhibit COX1, COX2, PGE2 (prostaglandin E2)
COX1 and COX2 produce PGE2
PGE2 stimulates mucous production and inhibits gastric acid secretion
so decrease in COX1, COX2, PGE2 leads to increase in acid secretion and decrease in protective mucous

102
Q

Examples of NSAID

A

aspirin
ibuprofen
naproxen

103
Q

What type of NSAID is aspirin

A

non-selective; blocks COX1 and COX2 but weakly more selective to COX1

104
Q

Use of aspirin

A

as an antiplatelet to prevent arterial thromboembolism

105
Q

Where does H. pylori usually colonize

A

antrum

106
Q

Symptoms of peptic ulcer

A

Epigastric pain
dyspepsia
nausea
heartburn

107
Q

Complications of peptic ulcer

A 
perforation
upper gi bleed 
gastric outlet obstruction (prevents gastric emptying) 
Duodenal obstruction
Peritonitis
108
Q

Which artery is usually eroded by duodenal ulcers

A

gastroduodenal artery

109
Q

Diagnosis of peptic ulcer

A

H. pylori testing
Bloods
Endoscopy

110
Q

Tests for H. pylori

A

Stool antigen test
Urease test
serology
culture

111
Q

Which 2 tests are the most common for H.pylori testing

A

Stool antigen test

Urease test

112
Q

How is urease test done and why is it done

A

done by taking a biopsy via endoscopy

It is done because H. pylori produces urease to increase pH of its environment

113
Q

What drug should be taken off from patients before H.pylori testing

A

PPI because PPI can give false negative results

114
Q

Why is serology not really used for H.pylori

A

Because it is not accurate with increasing patient age

115
Q

Management of peptic ulcer

A

Lifestyle management + Drug treatment

116
Q

What are the lifestyle advices for peptic ulcer disease

A

Avoid spicy / sour foods / caffeine
decrease alcohol consumption
smoking cessation
stop using NSAID

117
Q

What are the drug treatments

A 
If H.pylori positive 
- amoxicillin + clarithromycin + PPI (omeprazole) 
If penicillin allergic
- metronidazole + clarithromycin + PPI 
If H.pylori negative
- PPI for 4-8 weeks
118
Q

What dosage of PPI should be given to PUD patients

A

full dose ; omeprazole - 40mg a day

119
Q

Why is there poor compliance to triple therapy

A

Side effects: nausea, diarrhea

120
Q

Drug treatment if first line H.pylori eradication fails

A

amoxicillin + clarithromycin + tetracycline + PPI

If penicillin allergic
metronidazole + tetracycline / levofloxacin + bismuth + PPI

121
Q

Follow up management for PUD

A

Gastric ulcer - endoscopy after 6 - 8 weeks of PPi
duodenal ulcer - if no more symptoms - low dose PPI ; if symptoms persist - suspect malignancy / antibiotic resistance / rarer causes

122
Q

What are the causes of acute upper GI bleed

A 
peptic ulcer disease
gastric erosions
varices
oesophagitis
malignancy
Mallory weiss tear
123
Q

Which peptic ulcer disease most commonly causes upper GI bleed

A

duodenal ulcer

124
Q

What is mallory weiss tear

A

tear of lower oesophagus due to violent coughing or vomiting

125
Q

Symptoms of Upper GI bleed

A

Haematemesis
Malena (black, tarry stool)
signs of shock
syncope / confusion

126
Q

What is the 100 rule

A 
Represents symptoms that indicate poor prognosis for upper gi bleed
HR = <100 bpm
systolic BP = <100mmHg
Hb = <100 g/l
age = > 60
comorbidities
127
Q

What does systolic hypotension mean for shock

A

There has been loss of more than 30% of total blood volume, causing compensatory mechanisms to not function anymore

128
Q

Why should you keep an eye on young patients with upper GI bleed

A

They can compensate well initially but crash suddenly

129
Q

Upper GI bleed patients on beta blockers

A

will not show signs of tachycardia

130
Q

Upper GI bleed patients with diabetes

A

Poor autonomic response so may not show the signs

131
Q

Management of Upper GI bleed

A

Resuscitation
Endoscopy
treat underlying cause

132
Q

What are the resuscitation methods for upper GI bleed

A

ABCDE
IV fluid
blood transfusion

133
Q

Management for bleeding peptic ulcer

A

endoscopic treatment to attempt to stop bleeding

IV omeprazole

134
Q

What are the endoscopic treatments for bleeding peptic ulcers

A

Injection of adrenaline + Heater probe coagulation
Clips +/- adrenaline
Haemospray

135
Q

What solution of adrenaline should be used for injection in bleeding peptic ulcer

A

1 in 10000

136
Q

Effect of adrenaline

A

reduces blood flow to the area

137
Q

How does haemospray stop the bleeding

A

Soaks up water in the area, increasing concentration of coagulation factors

forms a barrier

138
Q

How many times should endoscopic treatment be attempted before surgery in bleeding peptic ulcers

A

2 times

Endoscopy -> IV omeprazole -> Endoscopy

139
Q

Post bleeding PUD management

A

Eradication of H. pylori if indicated

oral PPI

140
Q

What causes oesophageal varices

A

Portal hypertension (hypertension in the liver)
Portal hypertension makes it harder for blood to enter the liver then IVC so blood finds another way to flow back, which is through oesophageal vessels
This causes oesophageal vessels to dilate and become fragile

141
Q

What is the common cause of portal hypertension

A

Cirrhosis

142
Q

Resuscitation for bleeding oesophageal varices

A

ABCDE

IV fluids and blood transfusion

143
Q

Why should central venous pressure be monitored in bleeding oesophageal varices

A

It directly reflects the portal pressure. Needs to be monitored while giving fluid and blood to avoid raising the portal pressure

144
Q

How to stop the bleeding oesophageal varicse

A

Endoscopic variceal ligation (banding)
Sengstaken Blakemore tube
TIPSS

145
Q

Which scoring methods are used to assess the severity of haemorrhage

A

Blatchford

Rockall

146
Q

Effect of IV terlipressin

A

Causes sphlanchic vasoconstriction (vasoconstriction of sphlanchic vessels - SMA / IMA ..etc) to decrease blood flow

147
Q

When is TIPSS indicated

A

If endoscopic variceal ligation is ineffective

148
Q

When is Blatchford scoring used

A

After resuscitation of (first line assessment recommended by NICE)

149
Q

When is Sengstaken Blakemore indicated

A

If endoscopic haemostasis cannot be achieved or endoscopy is not availble
But this is not a definite treatment so if endoscopy fails, use TIPSS instead of this

150
Q

What is the first line method to stop variceal bleeding

A

Endoscopic variceal ligation (banding)

Y1 GI (6 decks)

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