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Management of GI and Endocrine Conditions > Lecture 2 - Peptic Ulcer Disease and GORD > Flashcards

Lecture 2 - Peptic Ulcer Disease and GORD Flashcards

1
Q

What percentage of the population suffer from dyspepsia anually?

A

40%

leads to primary care consultation in 5% and endoscopy in 1%

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2
Q

Of those who undergo endoscopy what percentage have GORD and PUD?

A

40% have GORD

13% havd PUD

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3
Q

What is dyspepsia?

A

A group of symptoms that alert doctors to consider disease of the upper GI tract

Dyspepsia itself is not a diagnosis

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4
Q

What are the symptoms of dyspepsia?

A

Upper abdominal pain or discomfort, heartburn, gastric reflux, nausea or voiting

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5
Q

What is GORD?

A

Gastro-oesophageal reflux disease

refers to endoscopically determines oesophagitis or endoscopy-negative reflux disease

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6
Q

What % of GORD and PUD sufferers self medicate?

A

50%

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7
Q

What percentage have cancer?

A

2% have gastric cancer

1% have oesophageal cancer

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8
Q

What are peptic ulcers?

A

Sores that develop in the lining of the stomach, lower oesophagus or small intestine

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9
Q

How much more frequent are duodenal ulcers than gastric ulcers?

A

10 times more frequent

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10
Q

What causes bleeding into the GI lumen?

A

damage to the blood vessels in tissues underlying the ulcer

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11
Q

What is a perforated ulcer?

A

When the ulcer penetrates the entire wall, resulting in leakage of the luminal content into the abdominal cavity

needs to be treated immediately - patient can die from infection

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12
Q

what % of patients with peptic ulcers suffer a perforation?

A

5-10%

this is higher in men than woman

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13
Q

What is the first sign of a perforated ulcer?

A

Sudden, intense, steady abdominal pain

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14
Q

How many patients die from perforated ulcer?

A

15%

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15
Q

Why do patients die from a perforated ulcer?

A

It enables the bacteria that live in your stomach to escape and infect the lining of the abdomen (peritoneum)

this is known as peritonitis

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16
Q

What happens in peritonitis?

A

the infection can rapidly spread in the blood (sepsis) before spreading to other organs

this carries the risk of organ failure and can be fatal if lest untreated

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17
Q

How does the mucosa protect the stomach from being digested?

A

The surface of the mucosa is lined with cells that secrete alkaline mucus that forms a thin layer over the luminal surface

both the protein content and its alkalinity neutralize H+ in the immediate area of the epithelium

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18
Q

What does the alkaline mucus form?

A

a chemical barrier between the highly acidic contents of the lumen and the cell surface

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19
Q

What do the tight junctions between epithelial cells do?

A

Limit the diffusion of H+ into the underlying tissue

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20
Q

How often are damaged epithelial cells replaced?

A

Every few days by new cells arising by the division of cells within gastric pits

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21
Q

What does peptic ulcer mean?

A

Ulcer of the stomach or duodenum

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22
Q

What does ulcer formation involve?

A

breaking down the mucosal barrier and exposing the uderlying tissue to the corrosive action of acid and pepsin

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23
Q

What are the characteristics of a peptic ulcer?

A

Epigastric pain that is relieved by antacids, nocturnal pain and vomiting

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24
Q

Who is peptic ulcer disease more common in?

A

Men and in smokers

there is often a family history of the disease

people who use NSAIDs or have a heavy alcohol intake

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25
Q

What ulceration are woman more likely to have?

A

Gastric rather than duodenal ulceration

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26
Q

What are gastric ulcers associated with?

A

the breakdown of the protective functions of the gastric mucosa, in association with normal or reduced acid secretion

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27
Q

What is duodenal ulceration accompanied by?

A

Excess acid secretion

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28
Q

What does the aetiology of PUD include

A

H. pylori, NSAIDs, pepsin, smoking, alcohol, bile acids, steroids, stress, changes in gastrin mucin consistency

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29
Q

What do the defence mechanisms include?

A

mucus, bicarbonate, mucosal blood flow and prostaglandins, cellular resitution and epithelial renewal

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30
Q

What can alter the mucosal defence?

A

NSAIDs, H. pylori infection, alcohol, bile salts, acid and pepsin

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31
Q

How do the factors alter the mucosal defence?

A

by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury

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32
Q

When was H. pylori linked to gastritis?

A

First in 1983

Since then, further study has revealed it is a major part of the triad which includes acid and pepsin that contributed to primary peptic ulcer disease

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33
Q

What type of bacteria is H. pylori?

A

Gram negative

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34
Q

What is duodenal ulceration?

A

A relapsing disorder, even after successful healing

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35
Q

What will a proportion of patients presenting with ulcer symptoms have?

A

gastric cancer, especially those over the age of 45

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36
Q

Why is investigation by endoscopy important in those above 45?

A

early drug treatment can produce symptomatic improvements in patients with early gastric cancer

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37
Q

What are peptic ulcers specifically?

A

defects in the gastric or duodenal mucosa that extend through the muscularis mucosa

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38
Q

What do epithelial cells of the stomach secrete?

A

Mucus in response to irritation and as a result of cholinergic stimulation

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39
Q

What does the superficial proportion of the gastric and duodenal mucosa exist as?

A

The form of a gel layer, which is impermeable to acid and pepsin

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40
Q

what do other gastric and duodenal cells secrete

A

bicarbonate, which aids in buffering acid that lies near the mucosa

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41
Q

what do prostaglandins do?

A

Prostaglandins of the E type, have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer

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42
Q

what are the 2 most important factors disrupting the balance between acid/pepsin attack

A

H. pylori and NSAIDs

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43
Q

What does H. pylori cause?

A

stimulates increased gastrin release and thereby increases acid secretion

it also causes direct damage to the mucosa, further disrupting the physiological balance

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44
Q

what do NSAIDs do?

A

impair the mucosal resistant, but do not alter acid secretion

patients taking NSAIDs do not produce prostaglandins

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45
Q

What % of peptic ulcers are caused by infection with H pylori or NSAID use

A

90%

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46
Q

What does inhibition of prostaglandin synthesis lead to?

A

a decrease in epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation and mucosal resistance to injury

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47
Q

What does lower mucosal resistance increase?

A

the incidence of injury by endogenous factors such as acid, pepsin and bile salts

as well as exogenous factors such as NSAIDs

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48
Q

How do NSAIDs cause peptic ulcer disease?

A

they disrupt the mucosal permeability barrier, rendering the mucosa vulnerable to injury

as many as 30% of adults taking NSAIDs have GI adverse effects

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49
Q

How does smoking affected PUD?

A

smoking is harmful to the gastroduodenal mucosa and H pylori infiltration is denser in the gastric antrum of smokers

cigarette smoke may increase susceptibility, diminish the gastric mucosal defensive factors or provide a more favourable milieu for H pylori infection

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50
Q

How does alcohol affect PUD?

A

ethanol is known to cause gastric mucosal irritation and nonspecific gastritis

evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive

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51
Q

What stressful conditions may cause PUD?

A

burns, CNS trauma, surgery, and severe medical illness

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52
Q

What increases the risk for secondary (stress) ulceration?

A

serious systemic illness, sepsis, hypotension, respiratory failure and multiple traumatic injuries

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53
Q

What can stress do once an ulcer is formed?

A

Emotional stress can aggravate the condition by increases acid secretion and also decreasing appetite and food intake

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54
Q

What are the causes of PUD

A

H. pylori infection, drugs (NSAID use), lifestyle factors (smoking, drinking), severe physiological stress, hypersecretory states (uncommon), genetic factors

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55
Q

What happens to basal acid output and maximal acid output in patients with duodenal ulcers?

A

In up to 1/3 of these patients, these are increased

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56
Q

How many patients have a family history of duodenal ulcers?

A

20% of patients have family history

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57
Q

What do the genetic factors relate to?

A

The production of mucin

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58
Q

what are the symptoms of a peptic ulcer?

A

Abdominal discomfort, pain or nausea
pain is located in the epigastrum and usually does not radiate

pain may be describes as burning, gnawing or hunger pains

classically gastric ulcer pain is aggravated by meals whereas duodenal ulcer is relived

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59
Q

what does pain radiating in the back suggest?

A

that an ulcer has penetrated posteriorly or the pain may be pancreatic in origin

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60
Q

what does pain radiating in the right upper quadrant suggest

A

disease of the gallbladder or bile ducts

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61
Q

how is the pain of peptic ulcer described

A

as burning or hunger pains slowly building up for 1-2 hours then gradually decreasing

antacids may provide temporary relief

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62
Q

why do patients with gastric ulcers present with weight loss?

A

because the pain is aggravated by meals so they avoid food

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63
Q

What alarm features warrant prompt gastroenterology referral?

A

bleeding, anaemia, early satiety, unexplained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, family history of GI cancer

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64
Q

what does documentation of PUD depend on

A

radiographic and endoscopic confirmation

an upper GI series is not as sensitive as endoscopy for establishing a diagnosis of small ulcers (< 0.5cm)

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65
Q

Diagnosis of an ulcer

A

endoscopy is not required unless the patient is present for the first time above the age of 55 or there are warning signs

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66
Q

What happens with people with dyspepsia with significant, acute GI bleeding?

A

they are referred immediately to a specialist

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67
Q

What is an endoscope?

A

a device used to diagnose gastric or duodenal ulcers, this uses fibre optic technology to visualise the mucosa

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68
Q

What is a biopsy?

A

samples of the tissue taken during the procedure

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69
Q

How big are ulcers?

A

usually range between 3mm and several centimeters in diameter

70
Q

When are X-rays good

A

when the ulcer is large and can be seen

71
Q

what % of individuals are infected with H pylori

A

40%

only some will develop disease

72
Q

how many patients with ulcers is H pylori seen in

A

95% of patients with gastric ulcer and 80% of those with duodenal

73
Q

Who won the Noble Prize for role of H pylori in gastritis?

A

Dr. Barry Marshall and Dr. Robin Warren

74
Q

What does H pylori survive in

A

a microaerophil

75
Q

Where does H pylori infect

A

the lower part of the stomach, the antrum

76
Q

what does H pylori cause

A

inflammation of the gastric mucosa (gastritis)

it is often asymptomatic

77
Q

What MAY H pylori result in

A

weakening of the mucosal defense systems, allowing for development of ulcer subsequent to acid/pepsin aggression

resides mainly within the gastric mucus and has a high activity of the enzyme urease which enables it to colonise in the stomach

78
Q

how does H pylori avoid the acidic interior of the stomach

A

H pylori uses its flagella to burrow into the mucus lining of the stomach to reach the epithelial cells underneath where the pH is more neutral

H pylori is able to sense the pH gradient in the mucus and move towards the less acidic region (chemotaxis)

79
Q

what does this movement to the more neutral environment do?

A

keeps the bacteria from being swept away into the lumen with the bacterias mucus environment, which is constantly moving from its site of creation at the epithelium to its dissolution at the lumen surface

80
Q

Where is H pylori found?

A

in the mucus, on the inner surface of the epithelium and occasionally inside the epithelial cells themselves

81
Q

how does H pylori adhere to cells?

A

by producing adhesions, which bind to lipids and carbs in the epithelial cell membrane

82
Q

What does BabA bind to?

A

the Lewis b antigen displayed on surface of stomach epithelial cells

83
Q

What does SabA bind to?

A

Increased levels of sialyl-Lewis x antigen expressed on gastric mucosa

84
Q

How else does H pylori avoid areas of low pH

A

it neutralises the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to CO2 and ammonia, the ammonia (which is basic) neutralises the stomach acid

85
Q

What does serologic evaluation do?

A

Looks for the presence of h pylori antibodies

this may reflect previous exposure to the antigen but not indicate present, active infection

86
Q

What are the invasive diagnostic techniques

A

gastric endoscopy and tissue biopsy

87
Q

What are the non-invasive techniques

A

serum, breath tests and stool samples

88
Q

What is the urea breath test?

A

is it based on the ability of H pylori to break down urea into CO2 and ammonia

the CO2 is absorbed from the stomach and eliminated in the breath

89
Q

How is the urea breath test carried out

A

Patients swallow a capsule containing urea and if H pylori is present in the stomach the urea is broken up and turned into CO2, the CO2 is then absorbed across the lining of the stomach ad into the blood, it then travels to the lungs where it is excreted in the breath

samples of exhaled breath are collected and the isotopic carbon in the exhaled CO2 is measured

90
Q

If the isotope of carbon is present?

A

it means H pylori is present in the stomach, if it is not found it means H pylori is not present

91
Q

What happens to the test once H pylori is treated?

A

the test changes from positive to negative

it provides evidence of the infection being present

it has high sensitivity and specificity

92
Q

Blood tests?

A

commonly used and if the patient has been infected they will have H pylori antibodies in the blood

it does not tell you if H pylori is present in the stomach

93
Q

Stool antigen test?

A

an enzyme immunoassay designed to detect H pylori in faecal specimens by measuring H pylori antigen released from organisms lining the stomach wall

it is an accurate tool to diagnose active H pylori infection and to establish eradication of the organism following treatment

94
Q

What is the most accurate non-invasive test?

A

faecal antigen is more accurate than antibody testing and less expensive that urea breath testing

95
Q

What happens if H pylori is not eradicated?

A

about 80% of gastric and duodenal ulcers will reoccur within a year

if H pylori is eradicated the recurrence rate is low

96
Q

what does the body of the stomach secrete?

A

mucus pepsinogen and HCl

it is thinned wall

97
Q

what does the antrum of the stomach secrete?

A

mucus pepsinogen and gastrin

98
Q

What is the antrum?

A

the lower portion of the stomach

it has a thick layer of smooth muscle and is responsible for mixing and grinding the stomach contents

99
Q

What do the glands in the antrum secrete?

A

they contain endocrine cells that secrete gastrin

100
Q

What do the opening of the gastric glands secrete?

A

Mucus

lining the wals of the glands are parietal cells, which secrete acid and intrinsic factor an chief cells which secrete pepsinogeen

101
Q

What are the unique invaginations?

A

an infolding of the outer layer of cells of a organism or part of an organism so as to form a pocket in the surface

102
Q

What do the invaginations of the luminal membranes do?

A

they increase the surface area for secretion, thereby maximising the secretion into the lumen of the stomach

called canaliculi

103
Q

What else do the gastrin glands of the antrum contain?

A

Enterochromaffin-like cells

and endocrine D cells

104
Q

What do enterochromaffin like cells release?

A

Histamine

105
Q

What do endocrine D cells secrete?

A

Somatostatin

these are located in and around the glands in the antral region

106
Q

What do histamine and somatostatin have roles in?

A

Regulating acid secretion by the stomach

107
Q

What drugs are used to treat PUD?

A

antacids, antisecretory agents, raising gastric pH (above 3) for a few hours per day, pharmacological treatments, eradication of H pylori

108
Q

What are antacids?

A

they are weak alkalis so they partly neutralise free acids in the stomach

they also stimulate mucosal repair mechanisms around ulcers, possibly by stimulating prostaglandin release

109
Q

What are antacids mainly used for?

A

Symptomatic relief in patients with PUD and GORD and non-ulcer dyspepsia

110
Q

What are antisecretory agents?

A

Drugs that inhibit gastric acid secretion

111
Q

How long must gastric pH be raised for to promote rapid healing?

A

For a minimum of 18-20 hours per day

112
Q

Raising gastric pH?

A

Need to raise it to more than 3 to promote healing and the duration of acid suppression will determine the rate of healing

113
Q

Name histamine receptor antagonists

A

cimetidine, ranitidine, nizatidine, famotidine

114
Q

How do H2 receptor antagonists work?

A

they are competitive antagonists for histamine at the H2 receptor found on parietal cells

by competing with histamine at the receptor, these drugs reduce acid secretion by the parietal cells

115
Q

When are H2 receptor antagonists best at reducing acid secretion?

A

At night and in the fasting state

116
Q

How effective are H2 receptor antagonists?

A

Bring about a 50% decrease in acid secretion for 10 hours, they are given twice daily

relapse is common after treatment

117
Q

How quickly can H2 antagonists heal duodenal ulcers?

A

~75-80% within 4 weeks of treatment and increases to ~90% by 8 weeks

118
Q

How quickly can H2 antagonists heal gastric ulcers?

A

It is slower, ~80% should heal by 8 weaks, this should be documented endoscopically

119
Q

Can H2 antagonists be used long term?

A

They can be continued as long term maintenance therapy however the role of these has been reduced since the important of H pylori infection has become appreciated

120
Q

Adverse effects of H2 antagonists?

A

diarrhoea, headache, confusion in elderly, gynaecomastia with cimetidine

121
Q

What is cimetidine?

A

A weak anti-androgenic (blocks the effect of dihydrotestosterone) in humans

122
Q

What does cimetidine inhibit?

A

cytochrome P450 system and has potential interactions with warfarin, phenytoin and theophylline as the half-lives of these drugs will be prolonged

123
Q

What has occurred after IV injections of H2 antagonists?

A

Some potentially serious cardiac dysrythmias

124
Q

Name some proton pump inhibitors

A

omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole

125
Q

How do PPI’s work?

A

they are irreversible inhibitors of the H+/K+ATPase pump and almost completely block acid secretion

126
Q

What does return of acid after PPI’s depend upon?

A

synthesis of new enzymes

127
Q

How do PPI’s bond to the pump?

A

they bind covalently via a disulphide bond thereby irreversibly inhibiting the proton pump

128
Q

When are PPI’s most effective?

A

when taken around meal times

129
Q

How effective are PPI’s?

A

Acid secretion is inhibited by ~90% for 24 hours after a single dose

130
Q

Adverse effects of PPI’s?

A

GI upset (epigastric discomfort, nausea, vomiting, diarrhoea), headache, skin rashes

131
Q

What is an adverse effect of omeprazole?

A

it has both stimulant and inhibitory effect on CYP450 system

132
Q

What does omeprazole reduce?

A

the elimination of diazepam, phenytoin and warfarin through inhibition of their heptatic metabolism

133
Q

What may long term use of PPI’s cause?

A

gastric atrophy or gastric cancers

this is due to substantial reduction of gastric acid and associated rise in gasrin secretion

134
Q

What else do PPI’s have a modest suppressant effect on?

A

H pylori

135
Q

What do patients with PUD testing +ve for H pylori infected get treated with?

A

Triple therapy - 7 day twice daily course of treatment

PPI, amoxicillin, either clarithromycin or metronidazole

136
Q

What is used as treatment in patients allergic to penicillin?

A

PPI, clarithromycin and metronidazole

7 day, twice daily

137
Q

What is recognised as an important factor in the failure to treat H pylori?

A

resistance to clarithromycin and metronidazole

138
Q

What are cytoprotective agents?

A

prostaglandin analogue (misoprostol), methyl analogue of prostaglandin E1, enhanced duodenal bicarbonate secretion, weak inhibition of gastric acid secretion, through activation of prostaglandin receptor on parietal cells, increased mucosal blood flow

139
Q

When can cytoprotective agents not be used?

A

In pregnancy - potential uterine stimulant and may induce aborption

140
Q

What is misoprostol?

A

A synthetic prostaglandin E analogue, which has an inhibitory effect on acid secretion and also enhances the secretion of bicarbonate, thus providing some additional protective properties

141
Q

What can misoprostol be used for?

A

To heal ulcers but is more commonly used prophylactically to prevent NSAID induced ulceration

142
Q

What happens in patients with an ulcer caused by NSAID?

A

the NSAID should be discontinued and patient given a H2 receptor antagonist

if the NSAID must be continues they should be given a PPI

143
Q

What does blood flow contribute to?

A

Protection by supplying the mucosa with oxygen and bicarbonate and by removing H+ and toxic agents diffusing from the lumen into the mucosa

144
Q

What is Zollonger-Ellison syndome?

A

A rare disorder that can cause gastric or duodenal ulcers (usually multiple) as well as in the jejunum

145
Q

What does Zollonger-Ellison syndrome cause?

A

massive gastric acid hyper-secretion due to gastrin secreting tumour in the pancreas or duodenum (gastrinoma) that stimulates acid secretion in the stomach

146
Q

When would you consider ZES?

A

if the patient has severe peptic ulceration, kidney stones, watery diarrhoea or malabsorption

147
Q

What can ZES be associated with?

A

multiple endocrine neoplasia type I, which occurs earlier tan isolated ZES

148
Q

What are patients with ZES likely to have?

A

Intractable ulcer disease

149
Q

What are patients with ZES serum gastrin levels?

A

usually have fasting serum gastrin levels of more than 200pg/ml and basal gastric acid hyper-secretion of more than 15mEg/h

150
Q

What must treatment of ZES do?

A

control the hyper-secretion and the gastrinoma

151
Q

What is the prevalence of GORD in the uk?

A

~20% of people in the UK experience symptoms once a week

152
Q

What is the increase of GORD due to?

A

Multi-factorial, though increasing obesity is an important factor

153
Q

What is acid secretion like in GORD?

A

most patients secrete a normal amount of acid, however they have an incompetent lower oesophageal sphincter that relaxes inappropriately at times other than swallowing

154
Q

What does the incompetent oesophageal sphincter allow?

A

excessive reflux of gastric contents, containing acid and pepsin, and bile acids into the oesophagus

155
Q

What is the tendency for reflux exacerbated by?

A

Hiatus hernia is present, since this further diminishes the barrier to reflux

156
Q

What are the symptoms of GORD?

A

retrosternal burning because the acidic material remains in contact with the mucosa for prolonged periods as a result of impaired physiological clearance mechanisms

157
Q

Drugs for treating GORD?

A

antacids and antacid/alginate combinations

drugs that inhibit gastric secretion (H2 antagonists and PPIs

drugs that act on oesophageal and/or gastric motility

158
Q

What happens when antacids are combined with alginates?

A

the alginate provides a protective coating to the lower oesophagus, reducing mucosal contact with the refluxed contents

159
Q

H2 antagonist use in GORD?

A

not particularly effective in the management of GORD, to be effective in GORD they need to be given at much higher doses than in PUD

160
Q

PPI use in GORD?

A

shown superior results compared to H2 antagonists in controlling symptoms and healing the oesophagitis

161
Q

Relapse in GORD?

A

relapse after treatment is common as GORD is a chronic condition and most patients require long-term treatment

most patients, especially with severe GORD require long term treatment with a PPI

patients with mild GORD may obtain sufficient symptoms relief from an antacid or H2 antagonist taken as required

162
Q

Drugs that increase gastric motility?

A

have some efficacy in patients with mild GORD because they have a weak tonic effect on the lower oesophageal sphincter and may also improve oesphageal clearance and gastric emptying

163
Q

Most frequent treatment for GORD?

A

PPIs

164
Q

When is surgery used for GORD?

A

in patients with severe, difficult to control GORD symptoms

may also be considered for people who have complications or scar tissue in the oesophagus

people who do not want to take medications for a long time

165
Q

How is surgery done for GORD?

A

using camera guided instruments

laparoscopic surgery requires smaller incisions than conventional surgery

166
Q

Nissen fundoplication?

A

excess stomach tissue is folded around the oesophagus and sewn in place

this holds extra pressure around the weakened oesophageal sphincter

167
Q

What is Barrett’s oesophagus?

A

an abnormal change in the cells of the lower portion of the oesophagus

the replacement of normal stratified squamous epithelium lining of the oesophagus by simple columnar epithelium with goblet cells (usually found in the lower GI tract where they secrete mucus)

168
Q

When is Barrett’s oesophagus commonly diagnosed?

A

in patients with long term GORD

169
Q

Diagnosis of barrett’s oesophagus?

A

rests upon seeing a pink oesophageal lining that extends a short distance up the oesophagus from the gastro-oesophageal junction

finding intestinal type cells (goblet cells) on the biopsy of the lining

170
Q

Symptoms of Barrett’s oesophagus?

A

most patients complain of heartburn pain, indigestion, blood in vomit or stool, difficulty swallowing solid foods or nocturnal regurgitation

171
Q

Treatment of Barrett’s oesophagus?

A

H2 antagonists and PPIs

controls symptoms but does not result in regression of Barrett’s oesophagus

172
Q

What is Barrett’s oesophagus associated with?

A

Increased risk of developing oesophageal cancer

Can lead to oesophageal adenocarcinoma (>85% mortality)

important to have checkups for precancerous cells and if they are discovered, they can be treated to prevent cancer

Management of GI and Endocrine Conditions (24 decks)

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