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CSI 8 Flashcards

1
Q

How long is the fibromuscular tube of the Oesophagus approximately?

A

25cm

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2
Q

Describe the path of the Oesophagus from where it originates to where it ends?

A

Origniates from the Inferior border of the cricoid cartilage (C6)

Descends downwards into the superior mediastinum of the thorax, positioned between the trachea and the vertebral bodies of T and T4.

It then enters the abdomen via the Oesophageal hiatus (opening in the the right side of the diaphragm) at T10

Terminates by joining the cardiac oriface of the stomach at level T11.

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3
Q

How long is the abdominal portion of the Oesophagus approximately?

A

1.25cm

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4
Q

What are the 4 layers of the Oesophagus?

A

Adventitia- outer layer of connective tissue ( but very distal and intraperitoneal portions of oesophagus have a outer serosa layer instead)

Muscle Layer-external layer of longitudinal muscle and inner layer of circular muscle.

Submusosa

Mucosa -Non-keratinised stratified squamos epithelium (contiguous with columnar epithelium of the stomach)

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5
Q

Describe the 3 layers of the exernal longitudinal layer of muscle in the oesophagus?

A

Superior third -voluntary striated muscle

Middle third- voluntary striated and smooth muscle

Inferior third- smooth muscle

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6
Q

How is food transported dpown the Oesophagus?

A

Peristalsis -rhythmic muscle contractions

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7
Q

What is dysphagia?

A

difficulty swallowing

can bne caused by hardening of muscles involved in peristalsis

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8
Q

What is the structure/location and function of the upper oesophageal sphincter?

A

Structure:

  • anatomical straited muscle sphincter at the junction between the pharynx and oesophagus
  • produced by the cricopharyngeal muscle

Function:

-to constrict(normally like this) to prevent the entry of air into the oesophagus

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9
Q

Location and function of the Lower oesophageal sphincter?

A

Location:

-Physiological sphincter located in the gastro-oesophageal junction(junction between the stomach and oesophagus tot he left of the T11 vertebra ), it is marked by the change from oesophageal to gastric mucosa

Function:

  • During Oesophageal peristalsis the sphincter is relaxed to allow food into the stomach
  • At rest the sphincter prevents the reflux of acidic gastric contents up into the Oesophagus
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10
Q

What is the structure of the lower oesophageal sphincter?

A

classified as a physiological (or functional) sphincter, as it does not have any specific sphincteric muscle. Instead, the sphincter is formed from four phenomena:

  • The oesophagus enters the 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 obstructing the lumen at the gastro-oesophageal junction.
  • The right crus of the diaphragm has a “pinch-cock” effect.
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11
Q

Where is food most likely to get stuck in the Oesophagus?

A

The anatomical relations of the Oesophagus which has given rise to 4 physiological constriction remembered as ABCD:

  • Arch of the Aorta
  • Bronchus
  • Cricoid cartilage
  • Diaphragmatic hiatus
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12
Q

What is Barretts Oesophagus?

What causes it?

A
  • Metaplasia of lower oesophageal squamous epithelium to gastric/intestinal columnar epithelium.
  • usually caused by chronic acid exposure due to malfunctioning lower oesophageal sphincter. The acid irritates the oesophageal epithelium, leading to a metaplastic change.
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13
Q

How can you detect barrets?

A

Endoscopy of the Oesophagus

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14
Q

What proportion of malignancies in the UK are oesophageal carcinomas?

A

2%

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15
Q

What are the clinical features of Oesophageal carcinomas?

A

Dysphagia- difficulty swallowing, becomes worse as tumour increase in size =restricts passage of food

Weight loss

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16
Q

What are the 2 major types of Oesophageal cancer?

A

Squamos cell carcinoma- most common type(occurs at any level of the oesphagus)

Adenocarcinoma- occurs in inferior third of the oesophagus.. It usually originates in the metaplastic epithelium of Barretts

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17
Q

What are oesophageal varices?

What is the problem with them?

A
  • Normally the abdominal oesophagus drains into systemic and portal vein circulation to form an anastomosis
  • varices are weird mini sub mucosal veins in the wall of the oesophagus that lies within the anastomosis
  • Usually made when portal hypertension happens ot their is blockage of the portal vein as the blood will then travel via the varices instead which is dangerous as these veins are weak can can burst.
  • Patients tend to present with haematemsis(vomiting blood).
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18
Q

What causes Oesophageal varices?

Who is at high risk of getting them ?

A

Causes- portal hypertension which is caused by chronic liver diseases such as cirrhosis

Alcoholics are at high risk

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19
Q

What is heartburn?

A

burning sensation in the chest because of acid reflux (stomah acid goes up oesophagus and into the mouth)

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20
Q

What is another term for reflux?

A

Gastro-oesophageal relux disease (GORD)

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21
Q

What is some treatmetn for reflux?

A
  • Proton Pump Inhibitor (PPI) for 4-8 weeks
  • H2 blocker(offered if PPI doesnt work)
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22
Q

What is the treatment for severe Oesophagitis?

A

Oesophagitis=severe inflammation

  • PPI for 8 weeks
  • If symptoms come back after you’ve stopped using PPI you should be given a higher dose or treatmetn with a different PPI. You may have to take treament for a long time
  • if it doesnt work your symptoms and lifestyle will be reviewed by GP and they may give a different PPI or get some specialist adivice e.g. a gastroenterologist
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23
Q

When is surgery for reflux and Oesophagitis appropriate?

What is the most common surgery for reflux and describe?

A

-For people who dont want to take medicine long term it have unpleasant side effects from medication

Laparoscopic fundoplication- A keyhole surgery technique, in which the surgeon stitches and folds the top of the stomach, just below where the oesophagus meets the stomach, to create a smaller opening. The aim is to reduce the amount of stomach contents re-entering the oesophagus.

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24
Q

What does the term dyspepsia encompass?

A
  • recurrent epigastric pain
  • heartburn
  • symptoms of acid regurgitation(with or without bloating)
  • nausea and vomitting
  • indigestion
  • tummy-ache
  • reflux
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25
Q
A
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26
Q

If Oesophageal reflux was a cause of a patients dyspepsia what additional symptoms might they experience?

A
  • belching
  • excess salivation in the mouth(water brash)
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27
Q

If gastroenteritis was the cause of the dypepsia what additional symptoms might occur?

A
  • Fevers
  • Vomiting
  • Diarrhoea
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28
Q

What are possible causes for dyspepsia?

A
  • Coeliac
  • Inflammatory Bowel disease
  • Upper GI malignancy
  • GORD
  • Gastritis
  • Pancreatitis
  • Medication Side Effects
  • Functional Dyspepsia
  • Gall Bladder disease
  • Gastroenteritis
  • Stress
  • Peptic Ulcer disease
  • Coronary Heart disease
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29
Q

What are the most common causes of dyspepsia in outpatients and what do they present with?

A

66% caused by functional dyspepsia-present with gastritis and normal results

19% caused by GORD-presents with Oesophagitis

13% caused by Peptic Ulcer disease- present with Duodenal ulcer and Gastric Ulcer

2% caused by Upper GI cancer - Gastric adenocarcinoma, Oesophageal cancer, Gastric Lymphoma

gastritis is pretty common and often resolves slef and may not always explain the symptoms opf dyspepsia

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30
Q

Why is the term functional dypepsia used to describe the cause of dyspepsia instead of gastritis?

A

In functional dyspepsia their is an element o gastritis present most of time but even if gastritis is present it does not correlate with the degree of symptoms which is why the term functional dyspepsia is attributed to the cause;

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31
Q

What can cause probelmatic and symptomatic gastritis?

A

when it is caused by:

  • infection
  • medication such as non-steroidal anti-inflammatory drugs which effects the integrity of theprotective mucus lining of the stomach
  • excess alcohol
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32
Q

Why is stress a risk factor of dyspepsia?

A

can be assosiated with functional dyspepsia, overt gastritis or peptic ulceration

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33
Q

What are common symptoms of GORD?

A

Discomfort particulary worse when eating especially after lying down and can feel like a burning pain behind the sternum

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34
Q

Describe colicky pain and its causes?

A

Colicky pain- refers to the type of intermittent, spasmodicpain that occurs when a hollow tube contracts to try and get rid of an obstruction. Things that cause colicky pain include Gallstones, renal stones and intestinal obstructions.

Gallbladder and billarty disease can presen tas dyspepsia but the pain is more of a colicky pain.

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35
Q

What are other possibilties to consider for causes of dyspepsia that are very unlikely but dangerous if missed?

A

Coronary disease-Mr muller has risk factors of this e/g stressful job and smoking. In some patients cardiac ischemia which would normally present as angina type pain can present as dyspepsia or atypical pain.

Due to this those with acute coronary syndrome with atypical symptoms are often misdiagnosed.

Also consider upper gastrointestinal malignancies which often present with dyspepsia

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36
Q

What is a red flag?

A

signs and symptoms found in a patients history and clinical exams that are indicators of a possible serious underlying condition.

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37
Q

What are red flags that might make a doctor think that someone with dyspepsia has upper GI cancer?

A
  • weight loss
  • haematemesis(vomited blood)
  • dyphagia
  • anaemia
  • upper abdominal pain with low haemoglobin level
  • raised platelet count
  • pain and vomitting may not be red flags if only for a couple of days as they might just be due to acute gastroenteritis, but if it were to persist for a long period of time without treatment particularly in over 55 =red flag
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38
Q

What 7 investigations should the GP conduct to find the cause of the dyspepsia?

A

Testing for H.Pylori, FBC, alcohol history, medication history, Weight, ECG, LFT’s(liver function tests)

This may vary based on the patient

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39
Q

Reasons to do each of the 7 tests to find the cause of dypepsia?

A

ECG- quick and non-invasive so good to look for cardiac abnormalities, get ECG done during the pain to see whether it was associated with cardiac ishchemia but an ECG could be useful regardless in highlighting old myocardial infarcts or other abnormalities.

Weight- simple and free, useful to have records on system to compare and monitor, good chance to calculate and discuss BMI

Alcohol history-recommended weekly limit is 14 units per week which Mr Muller is suggesting he may be above this, risk factor of dyspepsia, in excess can causes relevant problems like alcoholic gastritis or liver damage, regardless of its links to his current problem its important to discuss the risks of drinking to much with Mr Muller and advise and offer support if he’d like any.

Medication History- including any over the counter treatments might highlight medications that are contributing to dyspepsia such as those that can relax the oesophageal sphincter causing reflux (includes beta blockers, calcium channel blockers and nitrates) and those that can effect the gastric mucosa or it protective mucosa layer(nonsteroidal anti inflammatory drugs and aspirin)

Testing for H.Pylori – a bacteria that is commonly implicated in dyspepsia as it can cause a lot of the differentials e.g. gastritis, peptic ulcer disease and malignancies including adenocarcinoma and MALT Lymphoma (Mucosa associated lymphoid tissue). Infection with Helicobactor is highly prevalent and probably 50% of the worlds population have it living in their stomachs. It doesn’t always cause symptoms but if it does it needs treating.

FBC- need to know if he is anaemic and also if his platelets are high, both of which featured in the referral guidelines for suspected GI malignancy and are considered Red flags. A number of cancers can cause an elevated platelet count(thrombocytosis) due to release of cytokines that encourage platelet production. In GI cancers anaemia can occur due to occult blood loss because GI cancers are prone to bleeding and also because cancer cytokines can impact red blood cell production through interference with erythropoietin action.

Liver function tests-From Mr Mullers history Biliary disease is unlikely but not impossible, can show alcohol induced liver changes which could be considered an opportunistic test as it doesn’t bother him as he’ll be having blood test taken anyway.

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40
Q

Wht other investigations might be necessary to do to find the reason for the dyspepsia?

A

-stool sample(parasites, cysts and ova), stool sample(Microscopy, culture and sensitivities)- these my be more indicated if Mr Muller had diarrhoea, recent travel or a history more in keeping with gastroenteritis

-upper GI endoscopy(OGD-oesophago Gastro Duodenoscopy)- involves a camera being fed down the oesophagus and into the stomach where it gets a direct view of the upper GI tract as far as the beginning of the duodenum. This could be an essential investigation for certain people with dyspepsia however it requires a referral into secondary care, is invasive, often requires sedation and is not needed in everyone. Mr Muller has no features concerning enough to warrant an ODG at this time.

-digital rectal examination-used to look for evidence of upper gastrointestinal tract bleeding where it can identify presence of melaena (dark and offensive smelling faeces containing digestive blood from the upper GI tract, Mr Muller gives a really clear history and denies stool changes or vomiting blood so probs unnecessary. Rectal exam would be more relevant if a patient couldn’t answer those questions or in an acute scenario with an unwell patient

-Echocardiogram- may be relevant if his history showed more suspicions for cardiac involvement or if his ECG was abnormal, otherwise probs wont add much

-Abdomen radiograph-probs don’t need to do it on someone who presents as stable within the community, useful in an acute setting particularly when looking for an intestinal obstruction or perforation, but they don’t show more subtle findings in the soft tissues

CT Scan- probs wont help in Mr Mullers diagnosis, it is inconvenient, uses radiations and is expensive

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41
Q

What does H.Pylori do?

A
  • In the stomach there’s lots of HCL to kill pathogens
  • Foveolar cells in the stomach create an alkaline mucus to coat and protect the stomach linig from being corroded by the acid.
  • H.Pylori synthesises a molecule called ureases when it enters the stomach to neutralise the the acid surrounding it.
  • Urease converts urea into ammonia and CO2, ammonia is basic so can neutralise the acid surrounding H.Pylori to forma buffernig layer around it.
  • H.Pylori is not an acidophile so it swims to the musucs layer of the stomach where the pH is safer
  • It uses adhesion molecules to try to stick to the epithelial cells of the stomach lining e.g. Lipopolysaccharides(LPS) and BabA. The act of adherence itself is not harmful so the majority of people with H.Pylori in the stomach are going to be asymptomatic.

But some molecules in H.Pylori can turn it into a pathogen. A molecule called CagA disrupts the tight junctions between the epithelial cells in the stomach lining leading to an inflammation(lots of immune cells assemble at a certain site) because the site of inflammation is the stomach the inflammation is called gastritis.

  • vacA molecule form H.Pylori causes the cells in the epithelial cells in stomach lining to undergo apoptosis and die.
  • The combined effects of cagA and vacA can be bad as they both disrupt the stomach lining leading the underlying cells being exposed to the corrosive effects of gastric HCL which can lead to ulcers
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42
Q

What are the strains of H.Pylori?

A

cagA -ve or +ve

The +ve strains are more assosiated with gastric diseases

Not all stains are harmful and different people rect differently to different strains

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43
Q

What causes H.Pylori to go towards the stomach lining?

A
  • flagella propels it
  • guided by a chemotactic gradientn towards the stomach lining
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44
Q

When would you do a test for H.Pylori?

A

When patient has upper GI porblems

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45
Q

What are the 4 tests that test for H.Pylori?

A

Caron 13 urea breath test

stool antigen test

serum serology test

CLO Test

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46
Q

What are the pros and cons of the Carbon 13 urea breath test?

A

Pros:

  • Non-invasive
  • High sensitivity and specificity
  • can be used as a diagnosis and as a test of cure

CONS:

  • Requires specialist analysing equipment, samples may need sending away
  • If the patient is on antibiotics or PPIs the results might be falsely negative
  • requires fasting conditions
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47
Q

What are the Pros ans cons of the Stool antigen test?

A

PROS:

  • non-invasive, simple, safe
  • Hihg sensitivity and specifictiy
  • can be used for diagnosis and theoretically as a test of cure

CONS:

Patients might prefer other tests

  • samples need refrigeration
  • If the patient is on antibiotics or PPIs the results might be falselty negative
  • sufficient evidence lacking for use as a test of cure
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48
Q

What are the Pros ans cons of serum serology test?

A

PROS:

  • Cheap and wisely available
  • maybe useful for diagnosing a patient that is newly infected

CONS:

  • IgM poorly sensitive for new infection
  • IgG does not tell you if infection is current (as will remain positive after infection cleared)
  • cannot test for cure
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49
Q

What are the pros and cons of CLO test?

A

PROS:

  • high sensitivity and specificity
  • instantaneous results

CONS:

-If the pateint is on antibiotic or PPIs, the result might be falsely negative

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50
Q

Which of the H.Pylori tests does not probe for human genes?

A

Serology test

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51
Q

What do both the carbon 13 and CLO test test for?

A

presence of urease protein produced by H.Pylori

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52
Q

What does the stool antigen test check for?

A

The presence of antigens produced bhy H.Pylori particularly Catalase

53
Q

What does the serum antigen test check for?

A
  • the presence of specific human antibodies in the serum which have arisen due to the exposure of the H.Pylori antigens
  • However the exposure could have been in the past so a positive serum antibody result does not mean 100% that there is a current infection.
54
Q

What tests do NICE recommend for H.Pylori?

A

-the carbon 13 breath test or a stool antigen test

Both these tests possess high sensitivity and specificity and are non-invasive simple and safe. However the carbon 13 breath test also needs specialist equipment for sample collection. This may have been the reason the GP chose the stool antigen test over the carbon 13 breath test. But if the carbon 13 had of had any advantages over the stool test the GP would have chosen this despite that.

55
Q

Describe briefly the stomach lining?

What cells make HCL?

A

Gastric pits lead to gastric glands. One type of cell that lines the gastric glands is parietal cells. These secret HCL

56
Q

Describe how HCL is made?

A

On one side of the parietal cell you have the gastric gland leading to the lumen of the stomach, this is the apical side of the cell. On the other side of the parietal cell you have interstitial fluid with access to blood capillaries, this is the basolateral side.

1- CO2 molecules from the blood diffuse via the cell membrane on the basolateral into the parietal cell.

2-Carbonic anhydrase in the cell catalyses the conversion of this CO2 and H20 naturally inside the cell into carbonic acid which immediately dissociates into H+ and HCO3-.

3-Bicarbonate is exchanged for chloride via a Bicarbonate chloride antiporter on the basolateral membrane so chloride ions are now in the cell.

4-The H+ ion exits the cell on the apical side to enter the stomach lumen via a proton pump(gastric hydrogen potassium ATPase).

5-The pump exchanges the H+ for k+. There’s potassium outside due to pumps that previously transported potassium form inside to outside the cell.

6-Chloride channel on the apical membrane allows chloride from inside the cell to exit on the apical side. You know have h+ and cl- on the apical side(lumen) which leads to the production of HCL.

57
Q

Which receptors on the parietal cell help stimulate the production of HCL?

A

Ach receptors

H2 receptors which are a type of histamine receptor-initiate a signalling cascade that result in getting the proton pump from the cytoplasm to the apical cell membrane

gastrin receptors-

58
Q

What drugs help decrease the amount of HCL produced?

A
  • PPIs-also have a weak antibacterial effect against H.Pylori and anti-urease activity and anti-ATPase activity
  • H2 antagonists (inhibit H2 receptors)
  • Antacids(neutralises acid)
  • coupling PPIs with ABs will be more effective against H.Pylori as PPIs supress acid secretion causing ABs to concentrate thereby enhancign the effects of the ABs
  • Only 80% of acid secretion is blocked by PPIs so you may need H2 agonist as well
59
Q
A
60
Q

Give examples of PPIs, H2 antagonists ans antacids?

A

PPIS- Lansoprazole, Omeprazole

H2 antagonists-Cimetidine, Ranitidine

Antacids-aluminium hydroxide, magnesium carbonate

61
Q

Which H.Pylori test is validted by NICE as a test of cure?

A

Carbon 13 breath test

62
Q

Why can being on ABs and PPIs lead to false negatives?

How can it be avoided?

A
  • because the medicines effect the activity of H.pylori
  • only the serology one doesnt give a false negative
  • do the carbon 13 test after at least 2 weeks of no PPIs and 4 weeks of no ABs
63
Q

If H.pylorinhas cleared but dyspepsia is still presnet what is the protocol?

A
  • GP prescribes another 3 weeks of PPI omeprazole which in the case of gastritis often rleieves symptoms
  • when this doesnt help swith to another PPI e.g. ranitidine
  • If this doesnt work it means the patient has treatment resistant dyspepsia. MICE guidelines recommend GI endoscopy for this.
64
Q

What is another name for GI endoscopy?

A

(OGD) oesophago-gastro-duodenoscopy

65
Q

What is a hiatus hernia?

What are the risk factors?

What are the causes?

A

-occurs when part of the abdominal viscera herniate through the oesophageal opening in the diaphragm.

Risk factors-male gender, obesity, age, pregnancy and a genetic predisposition.

causes-widening of the diaphragmatic hiatus, pulling up of the stomach (e.g. due to oesophageal shortening) or pushing up of the stomach(e.g. due to increased intra-abdominal pressure)

the function of the lower oesophageal sphincter is compromised and the anti-reflux barrier is lost, allowing the stomach contents to reflux into the oesophagus. Therefore, hiatus hernias are a common cause of GORD

66
Q

What are the 2 types of hiatus hernias?

A

Sliding Hiatus Hernia:

  • 85-95% of cases
  • GOJ moves up
  • predominantly causes symptoms of GORD

Rolling Hiatus hernia:

-5-15% of cases

–GOJ remains in the same place

–A portion of the stomach, bowel, pancreas or spleen herniates into the chest next to the GOJ

67
Q
A
68
Q

Whats the difference between reflux and acid reflux?

A

acid reflux- stomach acid come up in the Oesophagus

Reflux- sometimes indigested food, goes up the oesophagus with the stomach acid and acts as a buffer to stomach acid to reflux is not always as acidic. This on-acid reflucx does not usually cause symptoms

69
Q

Why might you do a gastrooesophageal pH monitoring test?

A

To identift if a patient is suffering form acid reflux or non-acid reflux, as if they are suffering from non-acid reflux then PPI will not help

70
Q

How might you treat non-acid reflux?

A

use an alginate medication such as Gaviscon

-alginates precipitate into a gel which reacts with stomach contents to form a foamy raft which floats on top of the stomach contents, this can act s a barrier to reflux.

71
Q

What can happen to pateints with GORD?

A

10% of Patients with GORD can develop Barrets Oesophagus and 1-5% of people with this can develop Oesophageal cancer.

72
Q

What types of metaplasia are in Barrets and explain them?

A

Cardiac metaplasia - refers to tissue in the cardia part of the stomach being in the oesophagus.

Intestinal metaplasia - characterised by columnar epithelia and intestinal type goblet cells. Intestinal metaplasia may not be consistently distributed throughout the entire area of columnar lined oesophagus. Some areas may show cardiac metaplasia which is sometimes considered to be a precurser to intestinal metaplasia.

73
Q

What is the problem with the metaplastic cells in Barretts?

A

The non-native location of the cells mean the metaplastic cells are vunerable to developing architectural and cytological abnormalities.

74
Q

What is dysplasia?

What are the 2 types of dysplasia?

A

When cell abnormalities are confined to cells within the epithelium and above the basement membrane

High grade-more abnormal cells

Low grade-slighly abnormal cells

75
Q

What are other name for high grade dyplasia?

A
  • carcinoma in situ(a group of abnormal cells that remain in place where they first formed. They have not spread. These abnormal cells may become cancer and spread into nearby normal tissue),
  • intraepithelial neoplasia
  • stage zero cancer.
76
Q

Where else can high grade dyplasia/carcinoma in situ occur?

What are the risks?

A

ductal carcinoma in situ- occurs in the breast ducts

  • can also happen in the bladder, lungs, cervix and skin.
  • risk of deveolping into invasive cancer when the dysplastic cells extend beyond the their original location e.g. across the basement membrane.

This is why people with baretts are monitored every few years or frequently depending on status

77
Q

What are the possible treatmnt options for high grade dysplasia?

A
  • mucosal resection
  • radiofrequency ablation of the area
  • oesophagectomy
78
Q

What are some lifestyle changes (dos and dont’s) that can help ease heartburn and acid reflux?

A

DO:

  • eat smaller, more frequent meals(less acid production and less intra-abdominal pressure)
  • raise 1 end of your bed 10-20cm by putting something under your bed or matress - this elevates head and chest above waist so stomach acid does not travel up towards your throat
  • try to lose weight (increased weight on the abdomen can increase abdominal pressure = increase reflux)
  • try to find ways to relax (gut is connected to brain via brain-gut axis)

DONT:

  • have food or drink that triggers symptoms(spicy, citrus and coffee)
  • eat within 3-4 hours before bed
  • wear clothes that are tight around your waist (this can reduce pressure on abdomen= minimise reflux)
  • smoke
  • drink too much alcohol(could damge gastric mucosawhich may trigger acid production, inhibition or gastric emptying, could also cuase damage to oesophageal mucosa)
  • stop taking prescribed medicine without speaking to a doctor first
79
Q

What type of cells does an adenocarcinoma develop in?

A

Glandular cells in the Oesophagus

80
Q

How can stress effect GORD?

A

Stress can exacerbate symptoms of GORD by relaxing the oesophageal sphincter, slowing gastric emptying, increasing the susceptibility of the oesophagus to damage through changes to the inflammatory pathways and by increasing Oesophageal sensitivity to reflux material i.e. lowering the threshold for symptoms

81
Q
A
82
Q

What are the symptoms of Baretts?

A

no symptoms

But most people with Barrett’s oesophagus have symptoms of gastro-oesophageal reflux disease (GORD). The most common symptoms of GORD are heartburn and indigestion.

Other symptoms include: an unpleasant taste in the mouth, feeling sick (nausea), being sick (vomiting)

83
Q

What is the main cause of Barretts?

A

GORD-in some people the valve that joins the oesophagus to the stomach is weak. This means the stomach juice juices and acid come up into the oesophagus

84
Q

What increases your risk of developing reflux?

A
  • overweight
  • smoke
  • drink too much alcohol
  • eat spicy, acidic or fatty foods
  • hiatus hernia
  • men
  • people over 50
85
Q

What causes the metapasia in Barretts?

A

When cells in the Oesophagus come into contact with stomach acid during reflux over a long period of time

86
Q

What are the aims of treatment for Barretts?

A
  • reduce acid reflux and control symptoms
  • operation to strengthen valve at the bottom of the oesophagus
  • surgery to remove the effected area
87
Q

What are the differetn types of treatment for Barretts?

A

Surveilience-regularly monitiored e.g. regular endoscopies and biopsies. Aims to find early dysplasia that might cause cancer so trearment can be given immediately to prevent cancer/ cure early cancer.

Lifestyle changes-to reduce acid reflux. Eat small meals, dont eat 2-3 hours before bed, raise head of bed, avoid spicy and fatty food and alcohol. Kepp healthy weight, stop smoking.

Medicines to reduce reflux-PPIs, Hisamine antagonists. If symptoms improve dose is lowered to lowest dos ethat still helps. May have to take PPIs forever.

Fundoplication-operation to improve GORD. Done to repair hiatus hernia or strengthen valve at the bottom of the Oesophagus. Top of the stomach (fundus) is wrapped around the lower end Oesophagus and stitched into place= strnegthens valve and reduce reflux. Laproscope used for this keyhole surgery(small cuts instead of big). Bigger cut=laparotomy

Endoscopic mucosal resection(EMR)- removes the effected area of the oesophagus lining without damaging the rest of the oesophagus. Affected area removed using a thin wire called a snare which is put through an endoscope into the body.

Radiofrequency ablation (RFA)- uses heat to destroy abnormal cells Electrode probe down the Oesophagus and gives an electrical current to the abnormal area, which heats the abnormal cells to destroy (ablate) them. Anaesthetic needed and done in specialist centres so you need to travel for it. Cna have side effects e.g. feeling unwell, pain, high temp for a few days

Oesophagectomy- remove part of the Oesophagus if you have high grade dysplasia that can tbe removed via endoscope. After you will probs be in ICU for a bit, and be tube fed. May haev Nasogastric tube to remove digestive fluids to help area heal. Have x-ra to make sure join heals before eaitng.

88
Q

What new treatments are being tested for Barretts?

A

Multipolar electrocoagulation

cyrotherapy

89
Q

What is uninvestigated dyspepsia?

A

describes symptoms of pateitns who have not ye had a endoscopy to diagnose their dyspepsia

90
Q
A
91
Q

What is the cuase of dyspepsia symptoms in pregnancy?

A

usually GORD

92
Q

What is non drug treatment for dyspepsia?

A

healthy eating, weight loss (if obese), avoiding any trigger foods, eating smaller meals, eating the evening meal 3–4 hours before going to bed, raising the head of the bed, Smoking cessation, and reducing alcohol consumption may improve symptoms. Assess the patient for stress, anxiety, or depression, as these conditions may exacerbate symptoms

93
Q

When should an urgent endoscopic investigation be done on someone with dyspepsia?

A

Urgent endoscopic investigation is required for patients with dysphagia, significant acute gastrointestinal bleeding, or in those aged 55 years and over with unexplained weight loss and symptoms of upper abdominal pain, reflux or dyspepsia.

94
Q

What is the drug treatment for someone with functional or uninvestigated dyspepsia(consider if the patient is on aspirin or an NSAID-these make things worse)?

What treatment should be given to someone with refractory dyspepsia?

What treatment should be given if symptoms persist after initial treatment?

A

Antacids and/or alginates may be used for short-term symptom control, but long-term, continuous use is not recommended.

Initial management:

Uninvestigated dyspepsia-A proton pump inhibitor should be taken for 4 weeks. Patients with dyspepsia should be tested for Helicobacter pylori (H. pylori) infection, and treated if positive. Public Health England recommends that patients who are at high risk for H. pylori infection should be tested for H. pylori first, or in parallel with a course of proton pump inhibitor.

Functional dyspepsia- Patients should be tested for H. pylori infection and treated if positive. In patients not infected with H. pylori, a proton pump inhibitor or a histamine2-receptor antagonist (H2-receptor antagonist) should be taken for 4 weeks.

Follow up management:

For patients with refractory dyspepsia symptoms, new alarm symptoms should be assessed and alternative diagnoses should be considered. Check if the patient followed the initial management advice and reinforce lifestyle advice.

If symptoms persist or recur following initial management, a proton pump inhibitor or H2-receptor antagonist therapy should be used at the lowest dose needed to control symptoms. The patient may use the treatment on an ‘as-needed’ basis.

In patients with uninvestigated dyspepsia taking an NSAID and unable to stop the drug, consider reducing the NSAID dose and using long-term gastro-protection with acid suppression therapy, or using a different NSAID, such as paracetamol or a selective cyclo-oxygenase (COX)-2 inhibitor

In patients with uninvestigated dyspepsia taking aspirin and unable to stop the drug, consider switching from aspirin to an alternative antiplatelet drug.

Patients treated with H. pylori eradication therapy do not require routine retesting. There are specific situations where retesting may be appropriate, If retesting is positive, second-line eradication therapy should be prescribed.

Annual review for patients with dyspepsia to assess their symptoms and treatment. A ‘step down’ approach, or stopping treatment, should be encouraged if possible and clinically appropriate. A return to self-treatment with antacid and/or alginate therapy may be appropriate.

Referral to a specialist for further investigations should occur in patients of any age with gastro-oesophageal symptoms that are unexplained or non-responsive to treatment, or in patients with H. pylori infection that has not responded to second-line eradication therapy

95
Q

What are antacids for?

A

usually containing aluminium or magnesium compounds) can often relieve symptoms in ulcer dyspepsia and in non-erosive gastro-oesophageal reflux ; they are also sometimes used in functional (non-ulcer) dyspepsia but the evidence of benefit is uncertain

Conventional doses of liquid magnesium–aluminium antacids promote ulcer healing, but less well than antisecretory drugs;

Little proof that it’s neutralising capacity has the ability to heal

96
Q

When is it best to give antacids?

A

when symptoms occur or are expected, usually between meals and at bedtime, although additional doses may be required.

97
Q

What are magnesium and aluminium containing antacids usually for?

A

Magnesium-containing antacids tend to be laxative whereas aluminium-containing antacids may be constipating; antacids containing both magnesium and aluminium may reduce these colonic side-effects. Aluminium accumulation does not appear to be a risk if renal function is normal.

98
Q

What is sodium bicarbonate used for?

A

no longer be prescribed alone for the relief of dyspepsia but it is present as an ingredient in many indigestion remedies.

It is used in the management of urinary-tract disorders and acidosis.

99
Q

Why is bismuth not used for dyspepsia?

A

containing antacids (unless chelates) are not recommended because absorbed bismuth can be neurotoxic, causing encephalopathy; they tend to be constipating.

100
Q

Why are calcium containing antacids not prescribed for dyspepsia?

A

can induce rebound acid secretion

prolonged high doses also cause hypercalcaemia and alkalosis, and can precipitate the milk-alkali syndrome

101
Q

Why is simeticone(activated dimenticone) added to an antacid?

A

added to an antacid as an antifoaming agent to relieve flatulence and may be useful for the relief of hiccup in palliative care.

102
Q

Why are alginates taken in combo with antacids?

A

increases the viscosity of stomach contents and can protect the oesophageal mucosa from acid reflux. Some alginate-containing preparations form a viscous gel (‘raft’) that floats on the surface of the stomach contents, thereby reducing symptoms of reflux.

103
Q

What do PPIS do and briefly how do they work?

A

reduce acid secretion byirreversibly binding to H+/K+ adenosine triphosphatase, or the proton pump, located in the parietal cells. Thus decrease the amount of HCL made and secreted

104
Q
A
105
Q

When do we use PPI as treatment?

A

managing GERD, healing peptic ulcer disease, and reducing the incidence of nonsteroidal anti-inflammatory drug–associated gastropathy.

106
Q

What are 2 beneficial features of PPIs?

A

superb efficacy and low toxicity

107
Q

What is the probelm cuurrently with PPI prescribing and taking?

A

healthcare providers are often prescribing these agents for prolonged—even lifetime—use, and many patients are taking the OTC agents beyond the recommended course of therapy without any supervision.

108
Q

What are some potential adverse effects of using PPIs long term?

A

risk of fractures

hypomagnesemia

Clostridium difficile–associated diarrhea

vitamin B12 deficiency

acute interstitial nephritis (AIN)

cutaneous and systemic lupus erythematosus events

potential drug interaction

hypergastrinaemia, pnuemonia and dementia(not official but also concerns)

109
Q

How do PPIs lead to hypergastrinemia?

How can this be prevented?

What problems could hypergstrinemia cause?

A

Gastric acid suppression leads to hypergastrinemia=causes rebound hyperacidity; after discontinuing PPI therapy, patients may experience worsening GERD symptoms. To avoid this, PPIs should be slowly tapered.

hypergastrinemia can cause parietal cells to hypertrophy and enterochromaffin-like cells (ECL) to undergo hyperplasia. These effects may increase the risk for gastric cancer, but this relationship has mostly been observed in vitro and it not proven that PPIS = increased cancer risk

110
Q

How does using PPIs lead to community aquired pneumonia possibly?

Who is most at risk?

What can be done to help?

A

Acid suppression leads to an increase in gastric pH, allowing for the overgrowth of non-Helicobacter pylori bacteria in gastric juices, gastric mucosa, and the duodenum. This can lead to microaspiration and lung colonization. PPIs may also impair immune-defense mechanisms.

It is important to ensure that patients who are at risk for CAP, including the immunocompromised, elderly, smokers, and those with COPD and asthma, receive their annual influenza and recommended pneumococcal vaccinations.

111
Q

Why might PPI use cause an increased incidence of C.difficile colitis/infection?

Who is most at risk and how can we help?

A
  • due to a higher gastric pH, which could lead to a more virulent strain of bacteria.
  • The delay in gastric emptying can prolong exposure to the bacteria
  • immunocompromised, the elderly, hospitalized patients, and those taking broad-spectrum antibiotics; consider an H2-receptor antagonist as an alternative
112
Q
A
113
Q
A
114
Q
A
115
Q

Why might PPIs cause fractures?

How caan this be avoided?

A

A causal relationship has been noted between acid suppression and reduced absorption of mineral calcium in the diet; there may be as much as a 41% reduction in calcium absorption after 14 days of omeprazole therapy. Give a low dose of PPIs on patient who are at risk

116
Q

How can PPI use lead to hypomagnesemia?

What are the symptoms of hypomagnesemia?

How can it be prevented?

A

symptoms include muscle weakness and cramps, tetany, convulsions, arrhythmias, and hypotension. Patients may also present with secondary hypocalcemia and hypokalemia.

-usualy due to long term use

Baseline serum magnesium levels should be obtained prior to initiating long-term therapy and monitored periodically thereafter. Caution should be taken when coadministering with other agents that may lower magnesium levels, such as digoxin and diuretics

117
Q

Why might PPI use cause B12 defficiency?

How can it be helped?

Who has a higher prevelance of B12 defficiency?

A

Malabsorption of vitamin B12 may result from atrophic gastritis and achlorhydria, promoting bacterial overgrowth that allows for the increased digestion of cobalamin.

Most patients who consume a normal diet probably will not experience any significant B12 deficiency.

Routine screening of vitamin B12 may be considered in the elderly(high risk) or malnourished patients receiving long-term therapy, since this patient population has a higher prevalence of B12 deficiency

118
Q

What is Acute intestinal Nephritis and when does it start in relation to PPI usage?

What happens if you stop taking the PPIs?

What are the symptoms of Acute intestinal nephritis?

A

This is a humoral- and cell-mediated hypersensitivity reaction that can occur within days of therapy initiation and as long as 18 months thereafter. Upon discontinuation of the PPI, most patients spontaneously recovered.

Symptoms of AIN, including nausea, vomiting, fatigue, fever, and hematuria. The onset is usually insidious; PPI therapy should be discontinued if AIN develops

119
Q

Why might PPIs lead to dementia?

A

PPIs may increase the production and degradation of amyloid and bind to tau. reduced levels of vitamin B12 and other nutrients may also play a role in the increased risk of dementia

120
Q

What is drug induced lupus erythematosus (DILE)?

What is Subacute Cutaneous Lupus Erythematosus
(SCLE) and the symptoms?

What happens when you dicontinue the PPI?

Who is most at risk of SCLE?

A

Drug-induced lupus erythematosus (DILE) is a lupus-like syndrome that usually resolves after discontinuation of the medication.

SCLE is the most common DILE. Symptoms- annular and papulosquamous skin lesions, typically occurring on sun-exposed areas of the body, including the neck, back, shoulders, and upper extremities.

occurring anytime between 1 week and almost 4 years of PPI therapy. The resolution period after drug discontinuation was 3 months, on average, with no or minimal symptomatic therapy needed

At risk-including women of childbearing age, those with drug allergies or previous episodes of SCLE, photosensitive skin, exposure to ultra-violet radiation, and family history.

121
Q

How can PPIs effect other drugs, give examples?

A

PPIs reduce gastric acid production and raise gastric pH. Medications that require an acidic environment for absorption may have reduced efficiency in patients treated with PPIs. E.g. itraconazole, ketoconazole, isoniazid, oral iron supplements, and several protease inhibitors.

PPIs may inhibit the hepatic cytochromes involved in the metabolism of certain medications, raising concerns of additional drug interactions. Recently, attention has focused on the potential of PPIs to inhibit CYP2C19 and adversely affect the prodrug clopidogrel from being metabolized to its active form. Theoretically, such an interaction could reduce clopidogrel’s antiplatelet effect and lead to increased risk of cardiovascular events.

122
Q
A
123
Q

What are the available PPIs?

A

Currently, there are six PPIs available: dexlansoprazole (Dexilant), esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec), pantoprazole (Protonix), and rabeprazole (Aciphex). All are available by prescription. There are also products available OTC in both brand and generic forms, including Prevacid 24h, Nexium 24h, Prilosec OTC, and Zegerid (a combination of a PPI with an antacid).

124
Q

How should PPIs be taken?

A

generally speaking, these products are taken by mouth once daily, 30 to 60 minutes before breakfast.

125
Q

What minor side effects are assosiate with PPIs?

A

PPIs are generally well tolerated. The most common side effects reported include headache, diarrhea, nausea, and vomiting

126
Q

How long should you take PPIs?

A

OTC products should not be used for more than 2 weeks unless you are told to do so by your healthcare provider.

You should not abruptly discontinue the use of prescription products unless you are told to do so by your healthcare provider, since you may experience heartburn and other related stomach symptoms.

127
Q

How do the brain and the gut communicate?

A

via neural pathways- mainly involves the vagus nerve of the ANS interacting with the enteric nervous system

128
Q

What is the role of the gut microbiota?

A

The gut microbiota produces a huge range of chemical signals that can influence both the enteric and nervous systems

-also believed to play a key role in the development of the gut immune response. A healthy population of probiotic bacterial species is associated with a healthy immune system and an anti-inflammatory environment.

The endocrine and immune pathways are intertwined. For example, hormones such as cortisol and adrenaline influence the production of immune cytokines

129
Q

Describe how and why stress effects the gut and gut minrobiota?

Give an example of a gut disorder linked to stress?

A

Stress can influence the composition of our gastrointestinal bacteria. One mechanism for this may be due to altered levels of glucocorticoid hormones(due to stress), such as cortisol = leads to a modulated immune response whereby increased levels of proinflammatory cytokines alter the gut microbiota = change in the levels of neuroactive molecules released by gut bacteria = can directly/indirectly influence brain function and the subsequent interaction with the gut.

stress is well known to increase disease activity in inflammatory bowel disease and is also associated with a reduction in the concentration of aerobic bacteria such as Lactobacillus, a finding that is also commonly observed in inflammatory bowel disease.

CSI (5 decks)

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