Microbiology – Helicobacter Pylori (Ulcer)

Microbiology – Helicobacter Pylori (Ulcer)

In this video we are gonna look at helicobacter pylori The bacteria known to cause peptic ulcer as well as duodenal ulcer Helicobacter pylori is a Gram negative rod bacteria Here I am drawing sort of simplified structure of the bacteria H pylori has flagella which help in motility in moving around It also has DNA which is circular within it Some important vurulent factor that Helicobacter pylori possess include lipopolyscacrides which help in adhering to cells Another important virulent factor of H pylori is an enzyme on the surface known as urease Now urease is very important in Helicobacter pylori’s survival What urease does is that it converts urea and water to carbon dioxide and ammonia and this is important we will soon see why but essentially ammonia which is NH3 is quite basic so it’s alkaline and then H pylori can also secretes some exotoxin such as Vac A and Cag A Vac A essentially causes apoptosis of cells and then Cag A is responsible for disrupting the cellular integrity and structure and also promotes inflammation If that doesn’t all make sense dont worry hopefully we were able to understand after going through this video So H pylori is a common cause of peptic ulcer and duodenal ulcer Let’s just have a look at the anatomy of the stomach briefly and the GIT So here we have the stomach and the duodenum which is the first part of the small intestine Pyloric sphincter here is the barrier between the stomach and duodenum Anyway, the stomach has a few parts to it The fundus which is the top The cardia which is essentially the first part where the esophagus links the stomach The body and then we have the antrum The antrum is the most important part here because the antrum is where the H pylori resited and actually 50 percent of people have H pylori living inside them as commensal you can say commensal bacteria so zooming into the antrum the sromach we can see that the stomach cell are composed of columnar epithelial cells and the columnar epithelial cells they have a between them junctions known as tight junctions above this cloumnar epithelial cells we have a layer of mucus which are produced by the goblet cells (actually is epithelial cells) and mucus is very important because it acts a barrier from the hydrochloric acid a layer on top and the hydrochloric acid is important in the digestion of food The hydrochloric acid is produced by cells known as parietal cells and of course above this acidic layer we have lumen of the stomach resighting within the lumen of the stomach or just on top around here we have the bacteria H pylori and they could be here either through a infection or they could just be there normally because as I mentioned about 50 percent of people have H pylori within their stomach so just drawing it up we can see the pH decreases from the mucus layer up the top so the acid layer the hydrochloric acid layer is the most acidic so H pylori how does it survive in this acidic environment you see in the stomach you find the chemical urea and H pylori can convert urea to carbon dioxide and ammonia H pylori can do this because it has the enzyme urease and urease converts urea and water to carbon dioxide and ammonia and ammonia is sort of alkaline so it sorts of neutralises the acidity there and therefore the H pylori is able to move down towards the cells of the stomach and it can move down with the help of it’s flagella which helps in motility so two thing it’s doing it is using its enzyme urease to make ammonia which neutralises the acidity and the H pylori is using its flagella to help in moving down towards the stomach cells Once it makes contact with the stomach cells it can adhere to the stomach cells using lipopolysaccarides and once H pylori adheres to the stomach cells it can secrete this dangerous exotoxin such as Cag A and Vag A and as I mentioned Cag A disrupt cell integrity and essentially breaks down this tight junction between the stomach cells at the same time Cag A stimulates the productions of certain cytokines within its cells Cytokines such as IL- 8 so what does IL-8 do IL-8 is sort of like chemokine which tract neutrophil into the area and neutrophil is highly inflammatory it can damage essentially the stomach tissues so IL-8 promoted inflammation Now we have Vag A Vag A essentially induces or causes apoptosis of the stomach cells so the combination of Cag A and Vag A causes essentially just the breakage of the stomach cells and this essentially allows the hydrochoric acid layer and mucus layer on top to basically come in and as the hydrochloric acid layer comes in it will really damage and erupt the surrounding tissues and this is how the ulcer is formed it should be pointed out that the H pylori infection in the stomach which will promote inflammation will actually result in a lot more HCL acid being produced by the parietal cells and this is because inflammation essentially promotes HCL acid secretion in the stomach and with so much HCL being produced by the stomach the HCL can actually enter the duodenum which normally basic and so the H pylori infection can result in an duodenal cancer as well i hope this make sense now to diagnose a H pylori we will use a urea breath test a urea breath test essentially when a urea chemical is tagged the carbon of a urea chemical is tagged and then the person like basically eats the urea and then so the urea sample go down to the stomach where maybe the H pylori is if the H pylori is there the urea with water will be converted to carbon dioxide and ammonia and then the CO2 will actually have that chemical tagged on the carbon The CO2 will then leave the stomach to the bloodstream the CO2 will travel up to the heart and the heart will pump the blood with this chemically tagged carbon dioxide to the lung and then the CO2 will be exhaled out and so the presence of the chemically tagged CO2 will indicate that it is a H pylori infection others ways to diagnose H pylori infection include stool sample test now to treat H pylori infection you usually use proton pump inhibitor to prevent hypersecretion of HCL and you also use antibiotics to target the Hp

44 Replies to “Microbiology – Helicobacter Pylori (Ulcer)”

  1. Hi! I just wanted to know if you'd ever consider creating a book with all of your full drawings? Instead of or in addition of selling them one by one? 🙂

  2. PPI is taken to create an alkaline environment for the H.Pylori so it can undergo mitosis, in this state, it is most susceptible to the antibiotics.

  3. why h.pylori make no harm in some people and make serious disease in some people like atropic gastritis and cancer.

  4. Thank you so much for that explanation… my mom was just diagnosed with H pylori and stomach cancer. This video really help me understand her condition

  5. This was very helpfull as all the articles make this so complicated, but with the drawings it suddenly becomes very clear. Great video!

  6. The video is great I would have add the parietal cells and the H K ATPs pump , love your explanation, made it visual for me

  7. So i have erosive gastritis and before gastroscopy I have consumed food that helps heal gastritis or some natural remedies. So my question is: Can be H. Pylori missed on gastroscopy – biopsy test, or stool test becouse I have used 24 hours before test, something that might kill H. Pylori or heal gastritis in natural way?

  8. Doesn't inflamation involve the production/presence of protaglandins? isn't protaglandins cause inhibit parietal cell from releasing HCL? btw I did't learn this from school or what not so some term might be wrong.. so I'm sorry if I did any.

  9. Hi, i have some symptoms. Whatever i eat or drink.. i burp a lot. and also i am having hyper acidity with heart burn. But i did not feal any pain in my stomach.sometime My throat get tight and feal dificulty in breathing. Please tell me what could be this ?

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