CSI 8 Flashcards

Question

Answer 1

- belching - excess salivation in the mouth(water brash)

Answer 2

- Fevers - Vomiting - Diarrhoea

Answer 3

- 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

Answer 4

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

Answer 5

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;

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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.

Answer 10

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

Answer 11

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

Answer 12

- 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

Answer 13

Testing for H.Pylori, FBC, alcohol history, medication history, Weight, ECG, LFT’s(liver function tests) This may vary based on the patient

Answer 14

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.

Answer 15

**-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

Answer 16

- 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

Answer 17

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

Answer 18

- flagella propels it - guided by a chemotactic gradientn towards the stomach lining

Answer 19

When patient has upper GI porblems

Answer 20

Caron 13 urea breath test stool antigen test serum serology test CLO Test

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

PROS: - high sensitivity and specificity - instantaneous results CONS: -If the pateint is on antibiotic or PPIs, the result might be falsely negative

Answer 25

Serology test

Answer 26

presence of urease protein produced by H.Pylori

Answer 27

The presence of antigens produced bhy H.Pylori particularly Catalase

Answer 28

- 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.

Answer 29

-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.

Answer 30

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

Answer 31

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.

Answer 32

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-

Answer 33

- 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

Answer 34

PPIS- Lansoprazole, Omeprazole H2 antagonists-Cimetidine, Ranitidine Antacids-aluminium hydroxide, magnesium carbonate

Answer 35

Carbon 13 breath test

Answer 36

- 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

Answer 37

- 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.

Answer 38

(OGD) oesophago-gastro-duodenoscopy

Answer 39

-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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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.

Answer 44

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

Answer 45

**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.

Answer 46

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

Answer 47

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

Answer 48

- 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.

Answer 49

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

Answer 50

- mucosal resection - radiofrequency ablation of the area - oesophagectomy

Answer 51

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

Answer 52

Glandular cells in the Oesophagus

Answer 53

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

Answer 54

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)

Answer 55

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

Answer 56

- overweight - smoke - drink too much alcohol - eat spicy, acidic or fatty foods - hiatus hernia - men - people over 50

Answer 57

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

Answer 58

- reduce acid reflux and control symptoms - operation to strengthen valve at the bottom of the oesophagus - surgery to remove the effected area

Answer 59

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.

Answer 60

Multipolar electrocoagulation cyrotherapy

Answer 61

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

Answer 62

usually GORD

Answer 63

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

Answer 64

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.

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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.

Answer 69

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.

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

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.

Answer 74

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

Answer 75

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

Answer 76

superb efficacy and low toxicity

Answer 77

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.

Answer 78

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)

Answer 79

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

Answer 80

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.

Answer 81

- 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

Answer 82

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

Answer 83

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

Answer 84

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

Answer 85

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

Answer 86

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

Answer 87

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.

Answer 88

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. ## Footnote 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.

Answer 89

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).

Answer 90

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

Answer 91

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

Answer 92

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.

Answer 93

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

Answer 94

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

Answer 95

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.