GORD Flashcards
1
Q
Tell me what you can about mr Mueller?
A
- Belongs to private club where he drinks with clients- maybe he overdrinks
- finding it difficult to sleep, hence his girlfriend gave him a book on sleep solution
- he struggles to stop smoking
- his diet consists of takeaway
- his job is quite stressful; as he takes a lot of coffee a day but he has been promoted.
2
Q
What is the length of the oesophagus ? What is the function?
A
25cm.
it acts as a conduit for food (water and mucus) from pharynx into stomach
3
Q
What is the origin and end of the oesophagus ?
A
It originates at the inferior border of the cricoid cartilage (C6).
it ends at the cardiac orifice of the stomach (T11)
4
Q
At the origin of the oesophagus, what is it continuous supeirorly with?
A
It is continuously superiority with the laryngeal part of the pharynx ( the laryngopharynx )
5
Q
What portion of the thorax does the oesophagus enter? Where is the Oesophagus positioned in the thorax
A
It descends downwards into the superior mediastinum of the thorax.
It is positioned between the trachea and the vertebral bodies of T1 to T4.
6
Q
How does the oesophagus enter the abdomn
A
Via the oesophageal hiatus (an opening in the right crus of the diaphragm) at T10
7
Q
What is the length of the abdominal portion of the Oesophagus?
A
1.25 cm
8
Q
What are the layers of the oesophagus
A
Adventitia / serosa
muscularis externa
submucosa
mucosa
9
Q
What is Adventitia ? What part of the Oesophagus has serosa instead of Adventitia
A
Adventitia - outer layer of connective tissue.
it is the very distal and intraperitoneal part of the Oesophagus that has serosa instead of Adventitia.
10
Q
What are the layers of the muscularis externae and how do they differ in muscle type as you go down the Oesophagus
A
Outer longitudinal and inner circular .
Superior third of Oesophagus = voluntary striated muscle.
middle third - voluntary striated and smooth muscle.
inferior third - smooth muscle
11
Q
What does the mucosa of the Oesophagus contain
A
Non- keratinised stratified squamous epithelium ( it is continuous with columnar epithelium of the stomach)
lamina propria .
muscularis mucosa.
12
Q
How is food transported down through Oesophagus ?
A
Peristalsis- a rhythmic contractions of the muscles, which propagates down the Oesophagus.
13
Q
What can hardening of the muscular layers of Oesophagus lead to?
A
It can interfere with peristalsis and cause difficulty in swallowing (dysphagia)
14
Q
What are the oesophageal sphincters and their respective functions?
A
Upper and lower.
They act to prevent entry of air (upper) and reflux of gastric contents (lower)
15
Q
What are the features and functions of the upper oesophageal sphincters.
A
It is an anatomical, striated muscle sphincter at the junction between the pharynx and Oesophagus.
It is produced by the cricopharyngeus muscle.
Under normal conditions it is constricted to prevent entry of air into the Oesophagus
16
Q
What are the features of the lower oesophageal sphincters?
A
Physiological (functional ) sphincter located in gastro-oesophageal junction. The junction is situated to the left of the T11 vertebra.
The sphincter does not have any specific sphincteric muscle
17
Q
Where the location of the gastro-oesophageal junction and what marks it?
A
Situated at the left of the T11 vertebra.
Marked by change from oesophageal (stratified) to gastric mucosa (columnar epithelium)
18
Q
What are the 4 phenomena which forms the Lower oesophageal sphincter?
A
- The oesophagus enters stomach at an acute angle
- The walls of the intra-abdominal section of the oesophagus are compressed when there is a positive intra-abdominal pressure.
- The folds of mucosa present aid in occluding the lumen at the gastro-oesophageal junction.
- The right crus of the diaphragm has a “pinch-cock” effect.
19
Q
What situaitons are the sphincters relaxed or constricted?
A
It is relaxed during oesophageal peristalsis to allow food to enter stomach.
Otherwise it is constricted- what are the 2 functions?
20
Q
what is barretts oesophagus?
A
metaplasia (from stratified squamous to columnar epithelium) of lower oesophageal squamous epithelium
21
Q
What causes barretts oesophagus?
A
It is usually caused by chronic acid exposure as a result of a malfunctioning lower oepshageal sphincter.
The acid irritates the oesophageal epithelium, leading to a metaplastic change
22
Q
What is the most common symptoms for Barretts oesophagus ?
How can it be detected ?
A
Symptoms- long-term burning sensation of indigestion
it can be detected via endoscopy of the oesophagus (OGD). Patients who are found to have it will be monitored for any cancerous changes.
23
Q
What is the prevalence of oesophageal carcinomas
A
Around 2% of malignancies in the uk are oesophageal carcinomas.
24
Q
What are the clinical features of oesophageal carcinomas ?
A
Dysphagia- it becomes progressively worse over time as tumour increases in size, restricting the passage of food.
Weight loss.
25
What are the 2 major types of oesophageal carcinomas. Give features
Squamous cell carcinoma - most common subtype of oesophageal cancer. It can occur at any level of the oesophagus.
Adenocarcinoma- occurs in **lower 1/3** of Oesophagus. Associated with **Barrett's Oesophagus.** It usually originates in the metaplastic epithelium of Barretts Oesophagus
26
What 2 circulations does the abdominal Oesophagus drain into?
Systemic and portal circulation. Hence theres an anastomoses between the 2
27
What are oesophageal varices? And how does it normally occur?
They are abnormally dilated **sub-mucosal** veins (in walls of Oesophagus) that lie within this anastomosis.
They are usually produced when the pressure in the portal system increases beyond normal - **portal hypertension**
28
How does portal hypertension normally arise?q
It occurs (most commonly) secondary to chronic liver disease, such as **cirrhosis** or **obstruction in the portal vein.**
29
What group are at a high risk of developing oesophageal varices?
What does patients with varices commonly present with ?
Alcoholics.
they commonly present with haematemesis (vomiting of blood) ; the varices are pre-disposed to bleeding.
30
What do the anatomical relations of the oesophagus give rise to? Give its significance ?
The anatomical relations give rise to **4 physiological constrictions** in it's lumen.
It is these areas where food/foreign objects are most likely to become stuck .
31
What are the 4 physiological constrictions of Oesophagus anatomical relations - where food is likely to be stuck
* A- Arch of aorta
* B- Bronchus (left main stem)
* C- Cricoid cartilage
* D- Diaphragmatic hiatus
32
Below is a table of some anatomical relations of Oesophagus . Complete them
33
What is reflux ?
This is when some of the acidic stomach contents come back up the oesophagus towards the mouth.
It can also be called acid-reflux or GORD
34
When reflux occurs , what does the person feel and where can it be felt?
The person can feel heart burn- a burning sensation in the chest because of the acid in the stomach.
The pain is felt in the chest behind the breastbone and it may move up towards the throat.
35
Apart form heartburn, what other symptoms may be felt by someone with reflux?
Unpleasant taste in mouth .
swallowing problems.
36
Descirbe the treatment actions for someone with reflux
The GP should offer a course of PPI (proton pump inhibitor) for a course of 4-8 weeks. This depends on **severity** of the reflux and how **quickly your symptoms respond**.
37
What is the course of action for reflux if you stopped taking the PPI? (After course of treatment has finished then symptoms persist)
The GP should offer the PPI at the **lowest dose possible to control symptoms**. They should discuss taking it **only when you need it to help your symptoms.**
38
For reflux, what occurs if the PPI doesnt work? I.e. doesnt help at all.
The GP may offfer another medicine called a H2 blocker.
39
What is severe oesophagitis and what should the doctor prescribe if this occurs?
Oesophagitis occurs if reflux has caused severe irritation and inflammation of the Oesophagus.
The doctor should offer **PPI course for 8 weeks**
40
What is the next course of action if the symptoms (**oesophagitis**) come back after you've stopped taking the PPI?
The GP should offer a **higher** dose or treatment with a different PPI. You may need to take the treatment for a **long time to control the symptoms**
41
For Oesophagitis, what is the course of action if the PPI does NOT work ?
Doctor should do a systematic review of :
* symptoms
* lifestyle
* treatment.
The doctor may offer a different PPI or may wish to get a specialist advice (from a gastroenterologist)
42
What demographic of people is surgery approximate for? (Reflux or oesophgiis)
* People who do not want to take medication for a long term.
* Those who ave unpleasant side effects from their medication
43
What is the mos common type of surgery for reflux and describe what it entails
**Laparoscopic fundoplication**.
This is a key-hole surgery where the surgeon folds the top of the stomach (**fundus**) around the lower end of esopahgus and stitch it in place.
This occurs just below where the oesophagus meets the stomach ( a small opening is created).
This strengthens the LOS and can also repair hiatus hernia.
The aim of this is to reduce the amount of stomach contents re-entering the oesophagus
44
Should you keep taking antacids regularly for long periods of time? Give reasoning for your answer.
No, they may help with symptoms in the short - term but they won't cure the problem
45
In what way should doctors speak to help improve patients understanding?
Speak slowly, avoid jargon and repeat points.
The doctor should first establish what the patient knows and understands before launching into a discussion that begins at a level too complex or simple for the patient.
The overall aim is to ensure that they are communicating complex information in a clear and manageable way.
46
According to Gillian rowlands; what % of England's working age population struggled to understand health information that contained only text?
43%
47
Which demographics faced most difficulties in understanding health info by texts
* Older people
* black and ethnic minority groups
* those with low qualification
* those wihtout englsih as first language
* those with low job status
* those in poverty trap
48
What can poor skills in understanding and using health informaiton lead to?
They could leave patient at a higher risk of emergency admission to hospital and of serious health conditons.
49
In what ways does doctors use familiar words in unfamiliar ways?
Doctors may use the word chronic -meaning persistent. However, the patient may think it means severe.
the patient may not fully understand the meaning of the word or may be unfamiliar
50
What is dyspepsia?
Recurrent epigastric pain, heartburn or symptoms of acid regurgitation, with or without bloating, nausea or vomiting
51
Should you always use the term dyspepsia when talking to your patients ?
No, it depends on your assessment of the patient medical literacy. It is always better to use language in the terms that patients will understand.
This builds **trusts**
52
If the cause of dyspepsia was GORD, what other symptoms might a pt have apart from heartburn and indeigesiton
* Belching
* Excess salivation of the mouth
* nausea and vomitng
unpleasant tatse in the mouth.
53
What would be the symptoms if the cause of dyspepsia was gastroenteritis ?
* **Fever**
* vomiting
* belching
54
What were the most likely cause of dyspepsia in mr mueller case? What are the other causes?
5 most likely causes are:
* stress
* Functional dyspepsia
* gastritis
* peptic ulcer disease
* GORD
it is important to know what is more common (prevalence) and look at it in the context of the symptoms.
other causes:
55
What's the prevalence of the causes of dyspepsia normally presentable in pts
Functional dyspepsia - 66%
GORD- 19%
peptic ulcer disease - 13%
upper GI cancer - 2%
**add diagram**
N.b. Some pts with functional dyspepsia have gastritis
56
What are the features of functional dyspepsia ? What is present in investigations ? Give signicance
Symptoms of dyspepsia suffered but routine investigations doesnt show any causative abnormalities.
During endoscopy, elements of gastritis is revealed (70%).
\*However, the degree of dyspepsia doesnt correlate with amount of gastritis and hence it's still considered functional dyspepsia
57
What are the features of gastritis
Inflammation of gastric mucosa in which stomach lining is worn away.
it is quite common and it resolves by itself.
Some pts with it may not show dyspepsia symptoms.
58
However in some cases of gastritis, it is symptomatic. What are the causes of gastritis ?
* Infection
* alcohol excess
* Use of NSAIDS - they affect the integrity of the protective mucosa lining of the stomach
59
What can severe cases of gastritis lead to?
Ulceration
60
What are the 2 types of peptic ulcer disease and what is associated with ?
Gastric and duodenal ulcerations.
it can be associated with:
* functional dyspepsia
* overt gastritis
* peptic ulcerations- this is particular seen in pts in intensive care
61
If the cause of dyspepsia in pts is pancreatitis, what other symptoms will you expect to see?
Steatorrhea
IDDM
62
What is gallbladder disease and what do Pts with this normally present with?
Biliary disease. Pts present with ***colicky pain*** alongside dyspepsia.
63
What is colicky pain and how does it normally occur
Abdominal squeezing pain that tends to come and go in spasm -like waves.
It arises when a hollow tube tries to contract to relieve obstruction (that can be caused by gallstones)
64
What are the causes of obstruction that leads to collicky pain
Gallstones
Renal stones
Intestinal obstuction
65
What are the features of acute coronary syndrome in pts that present with dyspepsia?
Cardiac ischaemia that normally presents with angina type pain.
Sometimes pts may not present with angina type pain but only dyspepsia type pain- **atypical symptoms.**
**n.b. Uncommon diseases may often present with common symptoms**
66
When looking for differential diagnosis, some may be more dangerous. Hence what is the term for sassociated symptoms that indicate a more serious underlying pathology. Give significance
**Red flags**
they can be details in hostory or in clincal exams.
The more red flags you have, the higher the risk of having a serious pathology.
67
What is the course of actions for pts with lots of red flags. (For genral diseases)
They are prioritised quicker in mangement than those wihtout red flags
68
What are the serious condtions for pts presenting with back pain. Also give the corresponding red flags
69
What are the serious condtions and corresponding red flags for pts presenting wiht headaches
70
What are the red flags for upper GI cancer if the pt present with dyspepsia
* Dysphagia
* weight loss
* Haemetemesis
* Upper abdominal mass
* anaemia
* raised platelet count
Its important that some symptoms may not be immediately red flags but if they persist fro a long time despite treatment then its a red flag
71
What are the 7 most appropriate investigations for mr mueller ?
* Alcohol history
* H pylori test
* ECG
* liver function test
* full blood count
* medication history
* weight
72
Why is important to take an alcohol history for mr mueller ?
He might've drank Xs and needs advise and support.
To see if the past limits: 14 units a week spread out.
Alcohol is a risk factor for dyspepsia, alcoholic gastritis and liver damage.
73
What is it important to check ECG?
Can be used **during pain** to highlight where there's ischaemia
Can be used to see if there was an old myocardial infarction or other abnormalities
quick and non invasive
74
Why is it important to check the medication history in pets with dyspepsia ?
To check if pt is taking prescribed meds /over the counter meds that:
1. relax the lower oesophageal sphincter like:
* beta blockers
* calcium channels blokcers
* nitrates
2. those that affect the gastric mucosa (protective layer) like:
* aspirin
* NSAIDS
75
Why is it important to check for H.pylori in pts presenting with dyspepsia ?
Common for gastric malignancies like: adenocarcinoma or MALT lymphoma
It is highly prevalent (50%) of popul have it but it doesnt always cause symptoms but sometimes it does.
Very common in dyspepsia
76
Why is it important to check the full blood count for pets with dyspepsia
Look for red flags like:
1. **Anaemia** - due to **occult blood loss.** GI cancers are prone to bleeding. The cancer release ***cytokines*** that can impair red blood cells production **due to interference with erythropoietin action.**
2. ***High platelets*** - cancers release cytokines that promote platelet production.
77
Why is important to do liver function test for mr mueller ? And the wider pts presenting with dyspepsia
To look for biliary disease
To check for alcohol induced changes in liver.
It is an opportunistic test as it doesn't inconvenience him- he's going to need blood taken from him anyway.
78
Why do you carry out stool test for some pts with dyspepsia ? Why NOT for mr mueller in this case?
Not for Mr Mueller as there was no sign of diarrhoea or gastroenteritis.
Also Mr mueller didnt recently travel
Stool sample are taken to check for **MCS** and for parasites, cysts and ova
79
In what situation would you use an echocardiogram for pts presenting with dyspepsia
If ECG is abnormal
if there's history or suspicion of cardiac involvement
80
Why is CT scan not routinely used for pts presenting with dyspepsia
Expensive
Radiation
The results may not show suspected diagnosis
81
What is the purpose of doing a digital rectal exam for pts with dyspepsia. Why not in this case for Mr Mueller?
To check for upper GI cancer and Malaena.
This test is not relevant for mr mueller as he doesnt vomit blood and there's no stool changes
82
What is Malaena and how do it arise
Very dark and offensive smelling faeces.
It contains digested blood from upper GI tract in the faeces.
83
What is the features or OGD
Requires admission in secondary care
Requires sedation and its very invasive
its not for mr mueller at this time
84
Summarise the pathophysiology of H.pylori.
Due to urease , it is equipped to survive acidic conditions of stomach but it isn't an acidophile
It uses flagella to move into mucus layer above epithelial via chemotactic gradient.
It binds to epithelial via LPS/BabA.
Some strains of CagA positive H.pylori relases CagA that breaks down **tight junctions** between epithelial cells. This leads to gastritis
VacA is also released which causes apoptosis of cells lining the stomach
this leads to gastritis and ulcers
85
Why is that most people who have H.pylori are asymptomatic ?
The act of LPS/BabA binding to epithelial cells isn't harmful
not all H.Pylori have CagA
86
There are different tests fror H.pylori. Which ones are recommended by NICE to use as FIRST test for H.pylori ? give reasons
Carbon-13 urea breath test
Stool antigen test.
The GP (for mr mueller) chose the stool antigen test because carbon-13 test requires specialist equipment
87
Draw out the physiology of acid production in stomach and the treatment options (examples).
The H2 blocker stops the cytoplasmic tubulovesicels (with proto pump) to fuse weight the membrane.
It also stops the microvilli from projecting into canaliculi
88
Describe the effects of PPIs
Reduce acid production by 80%
PPI has anti-urease and anti-ATPase activity.
PPI has a weak antimicrobial effect and a weak eradication effect of H.pylori on it's own
89
Describe the effects of coupling PPIs with antibiotics or H2 blockers
Coupling with antibiotic potentiates the effects of the antibiotic and hence destroy bacteria. The PPI rescue acid production and hence concentrates the antibiotic in the stomach
Coupling PPI with H2 blockers will reduce acid production even more
90
Mr Mueller was give omeprazole, amoxicillin and clarithromycin.
He needs to be re-tested. What test is suitable for this and what conditions needs to be fulfilled?Give reasoning for this
Carbon -13 urea breath test is the **only** test validated by NICE for re-testing. its the only one that **tests for cure.**
Before retesting the pt should NOT take PPIs for 2 weeks.
Before re-testing the pt should not take antibiotics for 4 weeks.
This is because the medications affect the activity of H.pylori and hence can lead to false negatives in all tests EXCEPT serology. But serology test isn't useful as it cant test for cure.
91
After Mr Mueller was re-tested, he was negative for H. Pylori but he still had dyspepsia. What are is the next course of treatments and procedures
He was offered H2 blocker (ranitidine). After that, the dyspepsia persisted.
He has **treatment-resistant dyspepsia - this is a red flag for upper GI malignancy.**
He was then offered an OGD- he was found to have **hiatus hernia.**
The H.pylori was a red herring
92
What is hiatus hernia and how do they occur ?
This is when part of the abdominal viscera herniated through the oesophageal opening in the diaphragm.
They can occur via the following mechanisms:
* widening of the diaphragmatic hiatus or
* pulling up of the stomach due to oesophageal opening or
* pushing up of the stomach due to increased abdominal pressure
93
What are the risk factors for hiatus hernia ?
* Male
* age
* obesity
* pregnancy
* genetic predisposition
94
There are many mechanisms of hiatus hernia. What ultimately occurs due to the mechanisms
The lower oesophageal sphincter is compromised and the anti-reflux barrier is lost.
This allows the stomach contents to reflux into the oesophagus
95
What is hiatus hernia a common cause of?
what are the 2 variants of hiatus hernia ?
A common cause of GORD.
2 variants are:
1. Sliding
2. Rolling
96
What are the features of sliding hiatus hernia ?
They are present in 85-95% of cases
The gastro-oesophageal junction **moves upwards**.
It predominantly causes symptoms of GORD
97
What are the features of rolling hiatus hernia ?
5-15% of cases.
The gastro-oesophageal junction **remains in place**
A portion of the stomach , bowel, pancreas or spleen herniated into the chest next to the GOJ.
98
Normally, reflux is acidic. However, sometimes it's non-acidic. How does non-acidic reflux occurs and what monitoring does it need?
It occurs due to stomach food buffering the acid in the stomach
Non-acid reflux is **normally asymptomatic** but sometimes it can be symptomatic.
Non-acid reflux needs pH monthlong by the gastro team
99
What are the possible reasons for Mr mueller having treatment resistant dyspepsia
* Large hiatus hernia and insufficient acid suppression
* Functional dyspepsia
* Non-acid reflux
100
What is the treatment option for non-acid reflux. Explain how the treatment works
Use of ***Alginates*** like Gaviscon.
The alginates **precipitate into a gel that forms a foamy raft that floats on top of the stomach.**
This prevents acid reflux and acts as a physical barrier.
the sodium content and amount of additional ingredient/ antacid in individual preparation varies widely. Hence they are not easily interchangeable
The alginate itself could also reflux into the oesophagus instead of the irritation stomach contents- whether they may be acidic or non-acidic.
101
What is Barrett's oesophgus and how does it occur
what does it look like under the endoscopy ?
Metaplaisa from squamous to columnar.
some people (10%) with GORD will go on to have Barrett's Oesophagus
In OGD, Barrett's Oesophagus appear more red and velvety than normal Oesophagus .
102
What are the 2 types of metaplasia that occurs when you have Barrett's Oesophagus ? Contrast them
Cardiac and intestinal
intestinal metaplasia has goblets cells on it. It can occur in cardia of stomach or Oesophagus
Cardiac doesnt have any goblet cells. However it can progress to intesitnal metaplasia.
The gastro society accepts oth metaplsia has a diagnosis for Barrett's Oesophagus
103
What can Barrett's osoephagus lead to?
Low grade dysplasia - cells are slightly abnormal then it progress to -
***High grade dysplasia*** / carcinoma in-situ - more abnormal
this can then progress to invasive **adenocarcinoma. These can form a lump called tumour**
104
What's the difference between high grade dysplasia and adenocarcinoma in Barrett's Oesophagus
In high grade dysplasia, the dysplasia (neoplasm) ***hasn't pierce through the basement membrane*** and hence it's confines to cells above the basement membrane.
in adenocarcinoma, they have pierce the basement membrane and invaded nearby tissue
105
What are the management and treatment options for Barrett's oesophagus and dysplasia ?
Surveillance
Reducing acid reflux via lifestyle changes, surgery (fundoplication) and medications.
Removing the affected area via:
* Radio frequency abvlation
* Oesophagectomy
* mucosal resection
106
Where else can dysplasia occur part from Oesophagus?
* Bladder
* breast duct
* cervix
* skin
107
Most pts with GORD aren't monitored to see if they develop Barrett's . what criteria must they reach in order to be monitored?
Having history and family history of cancer
family history of Barrett's
108
Mr mueller was negative for Barrett's and dysplasia and he was given 20mg omeprazole twice a day.
What lifestyle changes does he need (most relevant to him) in order to get best outcomes
* Try to find ways to relax
* try to lose weight if overweight
* do not smokle
* do no drink too much alcohol
* do not eat within 3 or 4 hrs before bed
* raise 1 end of bed 10-20 cm by putting something under bed /mattress. Make it so that chest and head are above waist. This prevents reflux as gravity is doing the work
the other changes are in diagram - LEARN them although they're not relevant for Mr mueller
109
What types of food causes efflux? How do you make sure you monitor the food you eat and avoid types of food that causes reflux
* Spicy food
* Citrus
* Coffee
* Acidic food..
keep a diary of what you eat
110
Explain the effects of wearing tight clothes around waist on reflux
Increases pressure on abdomen and hence increases reflux
111
Descirbe the effects of alcohol on reflux
Chronic Alcohol excess lead to reflux by :
* destroying gastric mucosa which can lead to more acid production
* Inhibiting gastric emptying
* Reduce functions of oesophagus and lower oesophageal sphincter
* causing damage to Oesophagus
112
Explain how stress can exacerbate/ cause reflux
The CNS is connected to gut via brain-gut axis.
Exposure to stress can affect this axis and hence can exacerbate reflux by:
* relaxing the lower oesophageal sphincter
* slows gastric emptying
* reduce therehsold for reflux symptoms to occur
* increases susceptibitly of gastric mucosa to damage through changes to inflammatory pathways
113
How does smoking and high weight (BMI) causes reflux?
Smoking- nicotine relaxes the LOS
weight- high weight increases abdominal PRESSURE and increases chances of reflux.
114
What is the benefits of having lifestyle changes in response to dyspepsia
Lifestyle changes can reduce damage and symptoms of dyspepsia
it can also decrease your chance of developing Barrett's Oesophagus
115
Describe the pernitient features of stool antigen test .
give advantages and disadvantages
It looks for the presence of **H.pylori catalase (antigens)** in stool.
Can be used for diagnosis and theoretically as a test fro cure. However, not enough evidence to be used as a test fro cure
116
Descirbe the pernitent features of the CLO test.
give advantages and diasadvantages of this test.
Requires endoscopy and a biopsy is taken,
looks for the presence of urease enzymes.
It's invasive, however results are instantaneous
117
Give the pernitent features of serum serology test.
give advantages and disadvantages for this test
Looks for antibodies (IgG and IgM) produced against H.pylori.
A postive serum antibody test doesnt mean the infection is current.
Hence it cannot be used as a test for cure.
118
Give the pertinent features of carbon 13- urea breath test.
Give advantages and disadvantages
Patient take in tablets containing urea labelled with carbon 13. Then using a specialist equipment, breath is measured to look for activity carbon 13-isotope (after some time).
this test looks for presence/ activity of urease enzyme.
can be used as a test for cure.
Requires fasting conditions for 4hr at least
119
What is gastric pits and gastric glands
120
What's the prevalence of Barrett's oesophagus in the Uk and how many of them go on to develop cancer
1% of people have Barrett's Oesophagus
3% of people with Barrett's Oesophagus develop cancer.
121
If you have the common symptoms of GORD, for how long should they persist before you see your GP?
what are the symptoms that are red flags which you must tell your GP straight away?
2 weeks
Red flag symptoms are:
* dysphagia
* haemetemesis
* chest pain
* pain when swallowing food
122
What's the function of the diaphragm as partian to reflux
Helps to keep the acid and bile in the stomach
123
What demographic of people is Barrett's Oesophagus more common in?
* People who smoke
* men
* people aged over 50
it is also more likely in people who has severe reflux for years
124
Part of managing Barrett's Oesophagus is surveillance. Give me relevant features in which this entails?
This requires regular endoscopes and biopsies.
The aim of it is to find presence of dysplasia that can become cancerous. It's better to find it early so that treatment can start quickly to best [prevent cancer
the intervals between endoscopies depend on whether the cells are changing and the speed. It can be either 2 yrs or 3 months.
If symptoms gets worse/ you have new symptoms between appointment you should contact you doctor and don't wait for your appointment.
125
When biopsies show cells are still changing rapidly. The doctors may offer to remove the affected area by **Endoscopic mucosal resection**. Explain what this entails.
Using a thin wire called a **snare**, the surgeon removes the affected area of the ***oesophageal lining without damaging the rest of the oeophagus.***
The snare is in the endoscope
126
Describe the features of radio frequency ablation in removing affetced area of barrett's oesophagus. Include side effects.
An electrode is passed through an endoscope and it generates heat as current is passed through it. The heat ablates the abnormal cells.
it's usually done under genneral anasthetic. However sometimes local anaesthetic and some medication to make you drwosy is used.
Side effects of this interventions are:
* mild pain and discomfort
* unwell and high temperature in a few days
127
What are the NEWER treatments for Barrett's Oesophagus
* Multipolar electrocoagualtion.
* cryotherapay
they are only available as part of clinical trial. Not widely used.
128
Your doctor will only offer you an oesophagectomy if you meet these 2 criteria's. What are they?
1. You have high grade dysplasia
2. you have a high grade dysplasia that cannot be removed using an endoscope
129
Describe what oesophagectomy entails.
Surgeon remove part of Oesophagus containing abnormal cells.
Pt remain in ITU wirh drip inserted.
Nasogastric tube (from nose to stomahc/small intesitne) is added to remove digestiuve fluids. This helps the area to heal and stop you feeling sick.
the surgeon may put a small feeding tube directly into small intestine during the op and it'll help to feed until you recover. It is removed once you start getting enough nutrition by eating normally.
130
After an oesophagectomy, what may the pt feel? What are the limitations of the pt and how can that be mitigated until the pt returns to normal? Describe the process
Feel scared to swallow and have unwanted taste in mouth. Mouthwash help with th unwanted taste.
Can only take small sips of liquid until the join in of Oesophagus have started to heal. It'll take a few days before you can drink normally.
An x-ray is used to check for healing before you start eating. You start with small amount of food until you slowly build up to eating normally in a few weeks.
the feeding tube (if inserted) can be removed at this stage
131
What are the types of drugs that can cause dyspepsia ? How do you manage pts taking any of these drugs?
* Alpha blockers
* anti muscarinics
* benzodiazapines.
* CCB
* beta blocker.
* bisphosphonates
* corticosteroids
* nitrates
* NSAIDS
* theophylines
* tricyclic antideressants
they should be reviewed and the lowest dose should be used / if possible stop it.
132
Are antacids useful for long term continuous use? Why not? What other medication can be paired or substituted for antacids to perform it's role
No- only useful for short term symptoms
***alginates*** is the 2nd medication
133
whats the **initial** mamgament of **functional** dyspepsia
Test for H. Pylori and treat it using antibiotics if postive.
if negative, use PPI or H2 blockers
134
For follow up management for uninvestigated and functional dyspepsia. What should you do for pts with refractory dyspepsia symptoms ?
Assess for new alarm symptoms and alternative diagnosis should be considered
The pts adherence to initial management should be checked and lifestyle advice reinforced
135
For follow up management of uninvestigated and functional dyspepsia, what should you do if symptoms persist or recur following initial management
A PPI or H2 blocker therapy should be used at the lowest dose possible to control symptoms.
The pts may use the treatment on an 'as needed ' basis,
136
What should you do for pts with uninvestigated dyspesia taking NSAIDS and unable to stop the drug.
1. Consider reducing the NSAID dose and using the long-term gastro protection with acid suppression therapy OR
2. Swithicng to an alternative to the NSAID such as paracetamol or a selective COX-2 inhibitor
137
What should be offered to pts with uninvesitgated dyspepsia taking aspirin and unable to stop the drug
Consider switching to an **alternative antiplatelet drug**
138
Do pts treated with h.pylori eradication therapy needed routine retesting?
No , there are certain circumstance which it's needed.
if re-testing is postive, look at 2nd line eradication therapy
139
Descirbe the purpose of the annual review for pts with dyspepsia?
It is used to assess their symptoms and severity.
A step down approach or stopping treatment should be encouraged if possible and clinically appropriate.
A return to self- treatment with antacid/alginates therapy may be appropriate
140
What are the conditions in which referral to specialist is encouraged?
Referral for further investigations should occur in pts of any age withL:
* gastro-oesophageal symptoms that are unexplained or non-responsive to treatment
* H.pylori infection that hasn't responded to second line eradication therapy
141
Outline the initial management guidelines for uninvestigated dyspepsia
PPI taken for 4 weeks
Pts tested for h.pylori and if postive, treat it.
Patients at high risk of h .pylori infection should be tested for H.pylori first or in parallel with PPI treatment.
142
What is the role of **Simeticone** (in use of antacids)
Added to an antacid as an anti foaming agent to relive flatulence.
These preparations may be useful for the relief of hiccups in palliative care.
143
What is a healthy probiotic bacterial species associated with?
Healthy immune system and an anti-inflammatory environment
144
Draw and explain the brain gut axis
High levels of cortisol and SNS effects leads to a modulated immune response.
this leads to increased levels of proinflmmatory cytokines that alter the gut micorbiaota.
This leads to a change in neuroacitve molecules
This can then directly and indirectly affect the gut and the Brain function via an altered immune response.
145
How can stress increase disease activity of IBD?
what are the potential targets of future treatments that modify impact of stress on GI tract
Leads to reduction in lactobacillus
potential targets are:
1. target the Brain
2. target the gut microbiota - the gut flora is established a couple of years after birth
146
What are the adverse effects associated with long term therapy of PPI?
* Hypergastrineamia
* Pneumonia
* Dementia
* Drug interactions
* Risk of fractures.
* C.diffiicile diarrhoea
* B12 def
* Hypomagnesaemia
* Acute interstitial nephritis
* Cutaneous and systemic lupus erythematous events
147
Describe how long term use of PPI can lead to Hypergastrinemia ?
explain how to stop this and the other effects of hypergastrinemia
After stopping PPI there's **hyperacidity** - this leads to worsening GORD symptoms.
To avoid this the PPI should be slowly tapered.
in addition, hypergastrinemia lead to:
* hyper trophy of parietal cells
* hyperplasia of entero- chromaffin like cells.
this could lead to gastric cancer. This is normally ***in-vitro***; there's no strong evidence yet of long term use of PPI causing cancer.
148
How can long-term use of PPI lead to Community acquired Pneumonia ? What is the management of this scenario?
Acid suppression lead to increase in gastric pH.
this leads to non-H.pyloric bacteria in gastric juices, mucosa and duodenum.
This can lead to **micro aspiration** and lung colonisation.
PPI also compromises the immune system- evidence not conculsive
Mangement
* therapy not wihteld from those you suspect with having pulmonary disease.
* those with asthma, CAP, elderly and asthmatics recieve their influenza and pneumoccooal vaccine.
149
How can long term use of PPI cause c. Diff?
Lack of acid andf rediuced gastric emptying allows opportuntiy for a more virulent strain of bacteria to grow.
There has been more C.diff colitis in long term PPI users.
use PPI with caution in pts with:
* immunocompromised
* elderly
* hospitlaized
* taking broad spectrum antibiotics
use H2 antagonist instead
150
How can prolong use of PPI lead to fractures? How is this managed? What formulation is used?
Long term use of PPI could reduce absorption of calcium.
this leads to weaker bones and moreprone to fractures.
You can use calcium supplement in conjuction with PPI for those at risk of fractures.
Citrate formulations considered instead of carbonate to increase bioavalabilty
151
How can long term use of PPI lead to B12 deficeincy?
This occurs mainly in **eldery**. Those with normal diet of B12 will not be affected as much.
This deficiency could result from atrophic gastritis and lack of HCl.
Hence it promotes bacterial overgrowth and digestion of cobalamin
152
Descirbe the association between long term use of PPI and acute interstital nephritis?
Describe the symptoms and the features of this disease
This a humoral and cell mediated hypersensitivity - can occur within days or months after.
Upon stopping the PPI, most pts recover quickly.
Symptoms have an insidious onset and they are:
* nausea and vomiting
* fatigue
* fever
* **haematuria**
153
Describe how long term use of PPI can lead to dementia ?
PPI may increase the production and degradation of amyloid and bind to tau.
Also reduced levels of B12 could lead to increased risk of dementia
154
How can long term use of PPI be linked to SCLE? what demographics are at most risk of this side effect ?
There's **annular and papulosquamous skin lesion**s typically occuring on **sun-exposed areas of the body** including back, shoulders and upper extremities.
Most pts develop symptoms between 1 week and 4 yrs of PPI.
Group at most risk are:
* women of child bearing age
* drug allergies/ having previous SCLE
* having photosensitive skin
* family history
* exposure to UV rays
155
Describe how other drug interactions are affected due to use of PPI. What can u do about it?
Affects drugs that require **acid environmen**t like: ***isoniazid, oral ion supplement, protease inhibitors***, itraconazole and ketoconazole.
If alternative therapies cant be used, they should be advised to take the drugs towards end of PPI course.
PPI inhibit hepatic cytochromes involved in metabolism of certain drugs.
PPI inhibits CYP2C19 - stopping clopidogrel being metabolised into active form
156
Describe how long term use of PPI can lead to **Hypomagnesia**. Describe the symptoms and any other relevant features
Quite rare and life threatening but symptoms are:
* muscle weakness and cramps
* tetany
* convulsions
* arrythmias
* hypotension
* secondary hypocalcaemia and hypokalemia.
most cases are obtained when PPI therpay lasted 5 yrs.
Baseline magnesium levels should be obtained before long term PPI and then monitored after.
Take caution when administering digoxin or diuretics as they could reduce Mg levels
157
when can antacids be best used?
They are best used when symptoms occur or are expected -usulaly between meals and at bedtime.
Used for symptoms of ulcer in:
* functional dyspepsa
* Non-erosive GORD.
158
In what doses and forms are antacids best used ?
Coventional doses of liquid magnesioum-aluminium antacids promote ulcer healing but less well than antisecretory drugs.
Liquid preparations are more effective than tablet preparations
159
Give examples of antacids containing Al and Mg. Give their side effects and how can the side effects be reduced?
E.g. Are:
* Aluminium hydroxide
* magnesium carbonate
* Co-magaldrox
* Magnesium trisilicate.
they are relatively insoluble in water and hence long acting when retained in stomach
Mg are laxative. Al are constipative.
Use both together to reduce colonic side effects.
Al accumulation does not appear to be a risk if renal function is normal.
160
What does NICE say about using sodium bicarbonate in use fro relieve of dyspepsia ?
Can not be precribes alone for releif od dyspepsia.
it can be present as an ingredient in many indigesiton remedies
it is still useful for management of urinary tract disorders and acidosis
161
Explain the NICE guidelines on use of Bismuth -containg antacids and calcium containing antacids.
Not recommended
***Bismuth*** containing antacids (unless chelates) aren't ok to use. This is because bismuth can be neurotoxic- hence causing encelopathy.
They tend to be constipating as well.
***Calcium***- induce rebound acid secretion. Modest doses doesnt give significant results. high doses can cause hypercalcaemia and alkalosis.
it can also precipitate milk-alkali syndrome.
162
Does hydrotalcite give nay special advantage in treamtnent of dyspepsia symptoms?
No
using more than one antacid in preparation is the same as just using one antacid.
