My Pharmacology 3 experience

So I had pharma 3 yesterday. My examiner was prof. Gábor Pozsgai and he was very nice. I got two topics I liked and one which was meh, but I was hoping to get the 5 this time. In the end he asked me many things I couldn’t answer, and so I got a deserved 4.

There were four examiners who examined yesterday. Prof. Pozsgai, prof. Pethő, prof. Barthó and dr. Bölcskei. Prof. Helyes and prof. Pintér were not present.

You draw three topics, one from each pharma semester. My topics were “Local anaesthetics”, “Laxatives, antidiarrhoeal agents, drug treatment of inflammatory bowel disease and paralytic ileus, digestives, drugs used in cholelithiasis” and “Antiviral drugs against herpes, hepatitis and influenza viruses”.

As you might notice, my pharma 3 topic included influenza viruses, which, according to the topic list in the course information, should belong to the HIV topic. They moved influenza drugs from the HIV topic to the herpes and hepatitis topic.

Drug walk

My first question was to define potency. I defined potency correctly, but when I messed up when defining the ED50. I said that the ED50 is the concentration which gives the desired effect in 50% of patients, which is wrong. He told me that it was wrong, I corrected it and it was fine.

Then he asked me the differences between first and second generation antihistamines. I said that the first generation ones penetrate the BBB more easily, causing more sedation, and that the first generation ones block muscarinic receptors to a larger degree, causing side effects like dry mouth and constipation.

Then he asked me which drugs could be used in congestive heart failure. I said ACE inhibitors, AT2 antagonists, beta blockers, calcium channel sensitizers, cardiac glycosides and diuretics. He asked me what the indications for cardiac glycosides would be, as they’re not first-line agents. I didn’t know, but he said that they’re used if the patient has another condition in addition to the heart failure. I remembered that glycosides are anti-arrhythmics (even though I forgot to include them in the anti-arrhythmic topic, whoops), and so I said that maybe they would be preferred if there was also an arrhythmia. He said yes and asked which arrhythmia. With a qualified guess I said atrial fibrillation, which was correct.

Then he asked me to list the types of antianxiety and hypnotic drugs. I mentioned benzo’s, barbiturates and z-drugs. He asked me for a drug which is an anxiolytic but has no hypnotic effect. I asked if he meant any antidepressants, but that’s not what he was after. I remember that there were some atypical anxiolytics mentioned at the end of the benzo topic, but I couldn’t remember the name or the mechanism. He helped me by saying that it acts in a different manner than the other anxiolytics, but in the end I couldn’t produce the answer. He said that he was after buspirone. To be honest I had that name in my head when I was trying to find the answer, but I wasn’t sure so I never said it. Just goes to show that you should trust your gut.

He then asked me about the types of oral antidiabetics which don’t carry a risk for hypoglycaemia. I said metformin, GLP-1 agonists, DPP-4 inhibitors, SGLT-2 inhibitors and glitazones (I forgot the alpha-glucosidase inhibitors). He asked me which ones increase the risk for urinary tract infections, and I said the SGLT-2 inhibs. He asked me if I could name any, but I was honest with him and told him that I have given up trying to remember the names of the oral antidiabetics. It was fine, and we moved on to topics. He asked me which topic I wanted to start with.

Local anaesthetics

I wrote the spinal side effect thing on the bottom during the exam, so I could remember that he asked that.

I didn’t present the topic, he started by asking questions.

  • Examiner: What is the mechanism of action of local anaesthetics?
  • Me: They block sodium channels from the inside of the cell. They must diffuse into the cell, so they’re lipophilic. Inside the cell they’re ion-trapped, because these drugs are bases. This block is use-dependent.
  • E: What does it mean that it’s use-dependent?
  • M: It means that these drugs preferentially block the more active sodium channels.
  • E: What are the mechanisms behind this?
  • M: The drugs physically block the opening of the channels, so the more often the channels are open the more opportunities the drug has to plug it.
  • E: Yes, and there’s one more mechanism.
  • (I didn’t know that)
  • E: It has to do with its conformation.
  • M: Do they stabilize the channels in their inactive conformation?
  • E: No, not really.
  • M: Then I don’t know.
  • E: Okay, what can you say about the pharmacokinetics of these drugs?
  • M: Their effect is terminated when they’re absorbed into the systemic circulation.
  • E: Yes. Can you mention some side effects?
  • M: Yes, they’re bases so they can cause histamine release (I don’t know if this is true actually). They’re also cardiotoxic, so they can cause arrhythmia and negative heart effects.
  • E: Not really arrhythmias, but negative heart effects, yes. There are some special side effects when they’re given as spinal anaesthesia.
  • M: I don’t know.
  • E: They’re really characteristic side effects.
  • M: I don’t know.
  • E: Okay. Can you mention some local anaesthetics?
  • M: Yeah (I listed the ones I had written down).
  • E: Which is more long-acting, tetracaine or procaine?
  • M: Tetracaine. (Pure guess)
  • E: Yes. Do you know anything special about bupivacaine?
  • M: Hmm, I remembered prof. Gregus talked about the treatment of its intoxication.
  • E: Yes, what was that?
  • M: So bupivacaine is cardiotoxic, and if it’s injected into a vessel by accident it can be fatal. It’s lipophilic. By giving a lipid formulation like intralipid intravenously the lipid formulation can “dissolve” bupivacaine out of the heart.
  • E: Yes, do you know the original use of intralipid?
  • M: Yes, it’s used for parenteral feeding.
  • E: Yes, next topic.

Laxatives, antidiarrhoeal agents, drug treatment of inflammatory bowel disease and paralytic ileus, digestives, drugs used in cholelithiasis

I wrote the biological treatment of IBD during the exam
  • M: Okay, so we have four types of laxatives. Bulk laxatives, osmotic laxatives, faecal softeners and stimulant laxatives.
  • We talked a bit about laxatives, I don’t remember exactly what was said. I remember some of his questions
  • E: What’s another use for lactulose?
  • M: It’s used to treat hepatic encephalopathy.
  • E: And how does that work?
  • M: It acidifies the lumen of the GI tract, protonating ammonia to ammonium, preventing it from being absorbed.

I forgot the non-absorbable salts as osmotic laxatives. He tried to make me remember them by giving me some hints, but I had forgotten that they existed. He also talked about a faecal softener which is not on greek doctor and which I had never heard about. He also asked about the pharmacokinetics of senna glycosides, which I knew nothing about. Do they even have any pharmacokinetics? I also forgot adsorbents as antidiarrhoeal agents, and mebeverine.

  • E: Can you give me the drugs used to treat IBD? (funny, I was asked the same thing in pharma 2, and I have Crohn’s, so. Ironic)
  • I listed the ones I had written down, but while reading them I realized that I had forgotten to write down the biological treatment, but I remembed their name.
  • E: Which disease is the biological drugs more important in?
  • M: Crohn’s. (I’m actually going to start adalimumab in a few weeks)
  • He didn’t ask me anything else in this topic.

Antiviral drugs against herpes, hepatitis and influenza viruses

Notice how I messed up by forgetting gancyclovir, valgancyclovir and for saying that penciclovir and famciclovir are activated by UL97 kinase. I also forgot ribavirin when listing hep C drugs. I remembered it during the exam, but wrote it under the wrong hepatitis.

I began by listing drugs against herpes viruses. He asked about the mechanism of action of foscarnet. He asked me why we need prodrugs for these antivirals. Then he asked me about antivirals to treat EBV, or so I heard. I’m pretty sure I heard EBV, but I might have heard wrong, or he might have said wrong, because I’m pretty sure he was after ganciclovir and valganciclovir, which are used to treat CMV, not EBV. He asked me how antivirals are specific against virally infected cells.

  • E: What are the side effects of these drugs?
  • M: CNS toxicity? Hepatotoxicity?
  • E: No.
  • M: Nephrotoxicity?
  • E: Yes. How are these antivirals metabolized?
  • (I was pretty sure that they’re not metabolized but rather excreted renally unchanged. But I also didn’t think that he’d ask me a trick question like that, so I started guessing)
  • M: Are they metabolized by xanthine oxidase?
  • E: No, they don’t resemble nucleosides enough for that.
  • M: Then I don’t know.
  • E: They’re not metabolized, they’re excreted renally.
  • M: (jesus) So it was a trick question?
  • E: Yes (said with a stone cold face)

Then we went on to the hepatitis B drugs. He started by asking which hepatitises can be treated pharmacologically. I said B and C. I then listed the drugs I had written down.

  • E: What is the other use of these drugs?
  • M: Against HIV.
  • E: Yes. What’s different in the treatment of hep B and C?
  • M: The treatment of acute hepatitis C is curative.
  • E: Yes.

We went on to hepatitis C. I listed the drugs.

  • E: There is another drug which is very old, but still used. It might’ve been mentioned in other topics but it’s also used to treat hep C.
  • M: I don’t really know.
  • E: It causes some haematological side effects.
  • M: Ribavirin?
  • E: Yes.

He might have asked me some other questions about hep B and C, but I can’t remember now. We went on to influenza drugs.

  • M: Amantidine is used in influenza A. It inhibits an ion channel called M2, which is important for viral replication.
  • E: Can you be more precise about the step in the replication the M2 channel is important for?
  • M: No, not really. I don’t know.
  • E: Okay, continue.
  • M: We have oseltamivir, used for both influenza A and B. It inhibits neuraminidase, which is necessary for the release of the virus out of the cell.
  • E: Yes.
  • M: There is also baloxavir marboxil, which inhibits cap-endonuclease or something.
  • E: I’ve never heard of this drug.
  • M: Oh, haha. It was talked about in the seminar. It’s very recent I think.
  • E: Okay. There is a drug which has similar action to oseltamivir but has a very special way of administration.
  • M: Oh yeah. It starts with z, I don’t remember the name. It’s given by inhalation
  • E: I wouldn’t really say that it’s inhaled.
  • M: What? Then I don’t know.
  • E: It’s given by nasal spray.

It doesn’t say that on the seminar or in the book. It says that it’s given as a powder for oral inhalation, so he was definitely wrong about that.

And that was that. He spent a long time examining (especially compared to other examiners), but he was very nice.

Next

I have haematology on thursday and clinical biochem on monday.

I think greek.doctor is nearing its end. There aren’t any more subjects I want to write notes for, and I’m very, very tired of doing this. It takes a lot of time and energy, maybe more than most people think. Right now there are 817 pages, only maybe 10 of which aren’t topics and the vast majority of which I’ve written myself (the rest are written by my girlfriend, Sofia (msworldwide)). Almost all of these 817 pages are multiple pages long documents, and I spend maybe 2-3 hours per topic on average. I’ve been giving myself a lot of work by doing this, and I’m very glad that I did (maybe except for hema), but now I need time for myself to work on my mental health and engage in my hobbies.

I won’t take down the website. I’ll keep it up until it’s no longer used, which could be never. I’ll continue to maintain it by answering comments and fixing errors. I’ll post some statistics at the end of the exam period, as people seem to like that, and I think we’ll break the record again (like we do every exam period).

Oh, and by the way, I’ve made less than 5 euro from the advertisement on the page. I’ll keep it until the end of the exam period, but I’ll probably remove it as it’s not really worth having.

My Pharmacology 2 experience, some statistics and the future

So I had pharma 2 yesterday. My examiner was Dr. Kata Bölcskei, and she was extremely nice. My topics were “Anticoagulants and antiplatelets” and “Psychomotor stimulants and nootropic agents”. You draw two topics, one from each of two piles. The first pile contains topics 1 – 15, while the second pile contains topics 16 – 34.

I performed really poorly today, so thank god Kata is super nice. I hadn’t eaten today and I was tired, so I couldn’t really focus, neither when writing my topics or when answering her questions.

Drug walk

She started with the drug walk with all students. They consisted of three simple questions. Mine were:

  • Can you mention some preferential COX2 inhibitors?
  • Can you mention some drugs that are used to treat IBD?
  • Can you explain the mechanism of action of cardiac glycosides?

For the first question I didn’t quite catch that she said preferential and not selective, so I said celecoxib. I thought celecoxib was selective, but luckily for me it’s actually preferential, so she accepted it. And then I said “the other coxibs”, because I couldn’t remember the names, but then she said that they are selective and not preferential, and that’s when I understood that she wanted the preferential ones. I hadn’t really learned which are preferential and which are selective, so the only other one I knew was paracetamol. She wanted me to say one more, but I didn’t know. She was like “it starts with M.. melox..” but I couldn’t finish it because I had totally skipped that. It was meloxicam.

I was really glad when I got the second question, because I have Crohn’s and should know that. I still managed to forget one of the most important drugs, azathioprine, which I’ve even used myself… I listed corticosteroids, methotrexate, cyclosporin (not really used), rituximab (not really used), infliximab and adalimumab. I then said “the locally acting aspirins”, and then she asked me what the active compound of these drugs are. I answered acetylsalicylic acid, but she was like “but that’s aspirin. These are not aspirin. It’s not acetyl, it’s another chemical group that starts with A”. With that hint I managed to guess that it is aminosalicylic acid. I’ll have to correct that in the notes.

For the last question, I said that they inhibit the sodium potassium ATPase, causing more sodium to remain in the cell, which causes calcium influx which stimulates contractility.

That was the end of my drug walk. Other people were asked questions like “could you list me some synthetic/semisynthetic opioids, could you list me some serotonin agonists” and stuff like that.

Anticoagulants, antiplatelets

She begun by telling me that I don’t need to talk about antiplatelets, only anticoagulants, which was kind of weird and it sucked because I knew more about the antiplatelets than the anticoagulants. It might have been a blessing in disguise though, because I mixed up pentoxyfylline with dipyridamole.

I began by saying what I had written until I was done talking about coumarins. Then she started to ask me questions that I 100% definitely should know, but didn’t. It went like this:

  • Kata: “How long does it take for warfarins to be effective?”
  • Me: “One week”
  • K: “No, it’s just a couple of days. How do you administer warfarins?”
  • Me: “IV”
  • K: “That would only make sense if they were not orally absorbed, which they are. What else can you tell me about the distribution, elimination.”
  • After some help I remembered that they have high plasma protein binding, and that they’re eliminated by biotransformation.
  • K: “Yes. Which enzymes are involved in the biotransformation?”
  • At this point I was trying to remember which CYP enzyme it was, but I ended up just saying CYP enzymes and that was fine. She didn’t want the exact enzyme.
  • K: “What would happen to a patient if they were on warfarin but also on other drugs like valproate, or something” (She mentioned other drugs as well, don’t remember which ones.)
  • I caught on that we were talking about drugs that are CYP inducers, so I said that the warfarins would have decreased effect as they would be metabolised more quickly.
  • K: “And what would happen if a patient on warfarin one day for example ate a lot of vegetables”
  • Me: “They might consume more vitamin K and therefore decrease the effect of the warfarins”.
  • K: “Which parameters should be monitored for warfarin?”
  • I answered prothrombin time, which is correct but she said that the prothrombin time differs between laboratories because they use different methods, so we use a standardized measurement. I couldn’t remember it but of course the answer is INR. I couldn’t even remember what it stands for.
  • K: “How much should the INR be?”
  • I said 1.5, but it’s actually around 2.5 – 3.5

Then we finally started to talk about heparins. I said what I had written, and then she asked questions. She asked “So what is the route of administration for heparins?”. I said IV, which is true, but she wanted me to say subcutaneous as well (which I didn’t). I then talked about the LMWHs. She wanted me to mention specific names, but I couldn’t remember any. She tried to help me remember them by saying that they end in -parin, but I didn’t really remember them anyways.

She asked me what the rare adverse effect of heparins is, and I remembered heparin-induced thrombocytopaenia. She asked me what the treatment for this is. I answered fibrinolytics but appearently there are thrombin inhibitors that are given for this. I think the name was lepirudin, because she said it was a protein found in the saliva of leeches, but that drug isn’t mentioned on the lecture so idk.

Finally we moved on to psychomotor stimulants.

Yeah, I got the PDE inhibitor name wrong. At least pentoxyfilline is also a PDE inhibitor

Psychomotor stimulants

I began by reading what I had written down about amphetamines. She then asked me about the dangers of intoxication of amphetamines, which I hadn’t written down because I thought that was part of the drug abuse topics. I said stuff like excessive sympathetic activation, psychosis, potentially water intoxication, but I forgot hyperthermia.

I then proceeded with cocaine, saying what I had written down. She then asked me whether the effects of cocaine are similar or different than those of amphetamines, and I said they’re similar. She said that cocaine is also used as a topical vasoconstrictor during bleedings or something.

Then I said what I had written about the methylxanthines. She didn’t really ask me anything there.

Then she asked about dependence of psychomotor stimulants. I said that dependence is mostly psychological.

Finally we arrived at nootropic drugs. I explained what they are and what they are used for, and I mentioned the only example I remembered (memantine) and how it works. She asked me about other nootropic drugs, but I couldn’t remember any. She tried hard to help me remember them, by giving me the first letter or saying that the brand name is “Nootropil” and stuff. She said that some vinca alkaloids are used as nootropics, but I couldn’t remember the name.

After this she said that my anticoagulant topic was okay, but she had to help me a lot to remember stuff (she even said that other examiners might not have been as patient as she was..). The psychomotor stimulants was not so good, she said. She wanted to ask me more questions to get a 4.

She asked me if I could explain some mechanisms of action of antiepileptic drugs. I began with the most common one, the use-dependent inhibition of sodium channels. She wanted me to mention some drugs that use this mechanism. I said phenytoin and gabapentin, but she stopped me and said that gabapentin uses another mechanism. I said that gabapentin blocks calcium channels.

She asked for some antiepileptics whose mechanism of action involves GABA. I didn’t remember their names. She tried to help me remember by saying that they have “gaba” in their name, but I still couldn’t remember. She said that they are not so important anyway.

She asked about a newer antiepileptic drug which has much less side effects than others. I didn’t know, but I think the answer was lamotrigine.

She asked me to talk about the “Z-drugs”. I explained their mechanism and indications, and I mentioned zopiklon but forgot the name of zolpidem.

That was the end of it. She said that I should be able to produce more information on my own, without needing help to remember.

Closing thought about the exam

I got the 4 in the end, but to be honest I performed worse than I was expecting from myself so I don’t really feel that I deserve it.

I listened to exams before me, and trust me, you can get away with lacking knowledge about A LOT (like what sildenafil is..).

I know many are scared of the pharma 2 exam, and it’s probably mostly because it’s most people’s first oral pharmacology exam, so we don’t really know how the exam will be. I don’t know whether it’s possible to observe pharma exams like in anatomy, but if it is, maybe observing some exams can help you realize that they don’t require significant knowledge from your part. They mostly ask basic stuff, and even if you forget or don’t know some things, it’s perfectly fine. I know it may seem like my experience with Kata might not reflect how other examiners are, but I’ve heard that most examiners are very nice. I also think that Kata and Dr. Gábor Pozsgai examine most international students, and they’re both very nice.

Some statistics

Appearently people liked the statistics post from last semester, so I’ll do it again. I know it’s not the end of the exam period yet and there will probably be more statistics during week 7, but if I make this post after the exam period is finished no one will find it.

The peak on January the 7th is actually due to a robot spamming thousands of views on the hypertrophic cardiomyopathy preparation.

We broke a new record on visits and visitors on May 20th, with 7530 page visits and 338 visitors! Also, the total number of page visits since the inception has passed half a million! It’s fun to see how much more people use greek during the exam period than during the semester.

Most visitors are from Hungary of course, but there are quite a few from other countries as well.

People google stuff and end up here! That’s cool.

The most popular subjects are patho 2 and 1.

The last days there has been an average of 300 visitors and around 3000 visits.

502 comments have been approved, but that number includes my comments too. This means that you have posted 502-223 = 279 comments. Notice the huge amount of spam and trash (which is also spam).

The trash folder contains so much weird spam. Many of them try to sell drugs.

The future

I’m most likely going to apply to transfer to Semmelweis after the summer. Whether I get accepted or not remains to be seen, of course. I don’t know what the future of greek.doctor will be if I transfer, but I’ll keep you updated.

Good luck to those of you that still have exams!

My Microbiology 2 experience

I actually had Micro 2 last thursday, but I wasn’t planning to write about it until someone asked me to. I don’t really have much to say about it but here goes.

The exam is simple choice and there are 60 questions. There is no block system, unlike Micro 1.

I took Pathophys 2 monday the same week and therefore only had like 2.5 days to study micro. There was no reason not to try but I didn’t expect to pass. During this time I only watched and studied sketchy for bacteria, I didn’t study or look at any papers or notes. I quickly repeated some viruses as well. I didn’t have time to watch the fungi and parasite videos, so I was totally blank on those questions.

Luckily, most of the questions we got were bacteria-related, and most (but not all) could be answered with knowledge from sketchy. The virus-related questions were not very difficult in my opinion. There were some general microbiology questions and questions about diagnosis and such as well. If you’re curious about some of the questions, send me an e-mail and I’ll tell you what I remember.

In the end I barely got a 2 (with only 2 points to spare), so I definitely would not recommend skipping fungi and bacteria. I was lucky to pass at all with such short study time.

Good luck!

My Public Health 4 experience

I had Public Health 4 exam today. My examiner was Prof. Katalin Németh. She was very nice. There was a co-examiner present as well but I don’t know her name.

You draw 2 topics, one from the first half of the topic list and another from the second half. You then sit down and are given 15 minutes or more to prepare your topics.

My topics were “28. Epidemiology and prevention of enteric viral infections” and “12. Food additives”.

12. Food additives

I basically said everything I wrote down. They asked me if I could name some examples of how additives could increase the quality (like changing colour, taste, smell, consistency) and whether I knew what Chinese Restaurant Syndrome was (I didn’t tell them that initially). The examiners look at each other, shrugged 🤷‍♀️ and determined that there wasn’t much else to ask here.

28. Epidemiology and prevention of enteric viral infections

Once again I started by saying what I had written down. They asked a couple of questions:

  • Where else can you have outbreaks of norovirus? (Hospitals, kindergardens, schools)
  • How is the seasonality of these diseases? (Norovirus is more common in the winter)
  • What type of vaccine is the rotavirus vaccine? (Live attenuated, I answered wrong here)
  • When do we give the rotavirus vaccine? (Early after birth because it’s most fatal in infants and young children)

Result

I got a 5 and the exam was over relatively quickly. The examiner was super nice and the other students who had the exam at the same time had similar experiences.

I recommend you to take this exam after you’ve studied for micro 2 as there is significant overlap in the second half of the topics.

I made some very quick and dirty notes which you can download here. I didn’t have time to do the last 3 topics. These notes are based on the lectures, but for some topics there were no lectures available at Neptun so I had to collect information from other notes and the internet. Some of the topics are really short because I really don’t know what they expect (like carcinogenesis).

I think Lee misunderstood a couple of topics (like skin infections) so keep that in mind if you use his notes. I recommend using the lectures mostly as I’ve heard of people just reading Lee, Guro or other notes and ending up failing the exam because some topics are misunderstood there.

Next

Pharma is the only exam I have left, so I’m gonna start reading and writing those notes now.

My pathophysiology 2 experience

So I had pathophysiology 2 today. I had Professor Garai as my examiner. My topics were “Forms, general pathophysiology and consequences of anemia”, “Portal hypertension” and “Mechanisms and disturbances of bone remodeling. Osteoporosis, osteomalacia. “

Case

I began by presenting the case and my thoughts and explanations for each diagnosis, like this:

My case was a 64-year old female with established congestive heart failure. She had anasarca, shortness of breath on exertion and enlarged heart and spleen, polyuria at night and tachycardia in rest and during exercise. She also has arthritis and takes NSAIDs for the pain.

She recently experienced worsening of the heart failure symptoms. She also has occational gastric pain and decreased appetite. The blood parameters showed anaemia.

The case was that she had developed a gastric ulcer due to NSAID use, which had cause a chronic bleeding with resulting iron deficiency anaemia. This anaemia increased the demand for cardiac output, which worsened the heart failure.

His questions regarding the case were:

  • How would you treat this case?
    • Check and treat for H. pylori, give iron supplements, try to reduce the dose of the NSAID or switch to an NSAID that is less selective towards the isoform of COX which is present in the stomach (COX1) and more selective towards COX 2, which mediates inflammation
  • Which other drugs can you give for gastric ulcer?
    • Proton pump inhibitors, histamine antagonists, antacids
  • Why did anaemia cause worsening of the heart failure?
    • Anaemia increases the peripheral tissues’ demand for cardiac output, which the heart cannot provide when failing

ECG

I went through the ECG stepwise (like everyone should). There were no P-waves and there was absolute arrhytmia, indicating atrial fibrillation.

His questions were:

  • What is the most common cause of atrial fibrillation?
    • Hypoxia of the atria.
  • Which is caused by what?
    • Strain or increased load on the atria.
  • Which is caused by what?
    • Backward congestion of left or right-sided heart failure.

He also asked about some other findings of the ECG that I had mistakenly interpreted for scooped ST depression or deep S waves (which he absolutely didn’t like). They were instead descending ST depression in V4 – V6 and high voltage, indicating left ventricular hypertrophy.

Mechanisms and disturbances of bone remodeling. Osteoporosis, osteomalacia.

I explained everything I had written down. His questions were:

  • What is the third primary type of osteoporosis?
    • Juvenile osteoporosis
  • What else must you have in your diet to prevent bone mass loss?
    • Vitamin D
  • What other secondary causes of osteoporosis are important?
    • Chronic renal failure, hyperthyroidism, iatrogenic Cushing syndrome (I wrote down Cushing syndrome but I had said Cushing disease instead), hypoparathyroidism

He was particularly not happy with how I had just written down three causes for secondary osteoporosis when the list should be 50 diseases long.

Forms, general pathophysiology and consequences of anemia

I explained the different ways you can classify anaemias (according to etiology, morphology). His questions:

  • Which type of anaemia are you missing?
    • Aplastic anaemia
    • Also “anaemia of complex etiology”, but I didn’t know that
  • What is aplastic anaemia caused by?
    • Tumor infiltration of the bone marrow, radiation, osteopetrosis

He also asked me some causes of the different types.

Portal hypertension

I didn’t write down a lot here as I didn’t remember a lot at the top of my head. His questions:

  • What is the mechanism of portal encephalopathy?
    • Blood from the intestines containing ammonia, short chain fatty acids etc are shunted directly to the systemic circulation instead of through the liver
  • Where is the ammonia produced?
    • By enteric bacteria
  • Where else?
    • (The answer was the kidney but I didn’t know that)
  • How is ammonia toxic to the brain?
    • It increases the permeability of the blood brain barrier and it inhibits the TCA cycle
  • Which shunts do you have other than in the oesophagus and caput medusae?
    • I said in the rectum, but apperarently there are three more shunts that I didn’t know of

He also asked some questions about hepatorenal syndrome but I can’t remember what.

The stuff in the corner is unrelated

Closing thoughts

I got a 5 in the end, which I’m really proud of. He was really nice and patient, both with me and with the people before me. The assistant was nice and helped out too. If there’s something he wants you to say he will do everything to make you say it (which can take some time). Just don’t get discouraged if he says “Jesus christ” if you say something stupid.

He didn’t ask me many questions and my exam was over relatively quickly, but he did spend a lot of time with those before me. To be honest he didn’t ask me very difficult questions either, at least not compared to those he asked those before me. I couldn’t answer all his questions and many times he had to help me find the correct answer. I said some very wrong things about the ECG and the topics but he didn’t care too much as long as you correct them.

If you’re worried about pathophysiology, I understand, but believe me when I say that they’re very nice. They will most likely pass you if they see that you have studied, even though you don’t know all the mechanisms or details. If you’re really worried, consider being a witness to someone else’s exam so you can see for yourself how chill it is and how nice they are.

My Pathology 2 experience

It’s that time of the year again. I had my Pathology 2 exam today. Professor Tornóczki was my examiner. My topics were:

  • Benign and malignant tumors of the stomach
  • Tumors and tumor-like lesions of the liver
  • Slide: Paget disease of the breast
  • Prep: Mixed type testicular germ cell tumor

I loved my prep and slide but hated my theoretical topics. I wanted anything endocrine, IBD, male, female, skin or lung, but noo.. At least I didn’t get soft tissue, kidney or haema.

Benign and malignant tumors of the stomach

I begun talking about the adenocarcinoma. He liked most of what I talked about, but there were multiple questions I couldn’t answer. I said mostly everything written on the paper.

Here are some questions he asked that I couldn’t answer:

  • Except for smoking, gastritis and alcohol, what can be carcinogenic for the stomach (EBV)
  • Describe the pathogenesis of GIST (had no idea)
  • What is the carcinogenic component of H. pylori (CagA)

Tumors and tumor-like lesions of the liver

I begun talking about the hepatocellular carcinoma. He asked what can cause HCC without cirrhosis, I answered fibrolamellar type and aflatoxin. He asked what is characteristic for aflatoxin, to which I didn’t know. Appearently it gives a very characteristic “signature” mutation of the p53 gene (which I wrote on the paper after he said it).

He asked about the benign version of HCC, which I’d forgotten to mention or write.

He asked how one can get multiple echinococcus cysts. I didn’t know, but appearently the parasites can spread through the bile ducts before they die, forming multiple cysts.

We did not talk about cholangiocellular cc, liver abscess or liver cysts (other than the echinococcus).

Testicular mixed tumor

Of course I get the prep that teachers disagree about, and of course my teacher and my examiner disagree about it. I wanted to make it clear that there is a disagreement between teachers about which tumor is which, but he didn’t really let me. He also said that seminomas not rarely have haemorrhage and necrosis. I said that I think the bottom tumor is the seminoma and he disagreed.

I love testicular tumors and wanted to talk about a lot of theory here (as you can see from my paper), but he was only interested in the macroscopy.

I forgot to say that the testicle is enlarged (which is obvious), which I think might have disappointed him a little. I also didn’t know that testicular tumors cause painless enlargement, which is also important (and I’d forgotten).

It’s obvious I was eager to talk about theory here

Paget disease of the breast

Generally okay, however he disagreed that we can’t see the primary tumor in the slide as he showed me some atypical cells in one of the ducts. He also asked what Paget disease can look like, and appearently the answer is eczema (I didn’t know).

Like for the prep he was not interested in any theoretical knowledge here, which was unfortunate for me.

Overall

I got a 3 in the end. I got 3 on 3 of my topics and 4 on one of them, can’t remember which one. The theoretical topics weren’t my best picks and I do believe I could’ve gotten a better grade with better topics, but there were many of his questions that I couldn’t answer. In my opinion he was a little strict when he gave me 3 instead of a 4, but I’m just glad I passed.

He was very nice and his questions were for the most part easy to understand. I answered wrong or “I don’t know” to most of the questions he asked me. I wouldn’t worry if you get him as your examiner.

Good luck with your exams!

Please answer this questionnaire

The EGSC and HÖK have published a questionnaire regarding quality changes of the theoretical education. It asks questions regarding the biochemistry curriculum, midterms and the quality of lectures, among other things. There is a text box where you can write any improvements you have. Please take 5 minutes to answer it truthfully. You can find it here.

Here are some of my points for improvement. If you agree, please write it in the questionnaire:

  • Many lecturers are really bad at lecturing and making powerpoints and should undergo training or at least receive help when making the powerpoints.
  • It should be compulsory for lecturers to publish the PowerPoints, and this should be done before the lecture itself.
  • Lectures should be recorded and published so that students can rewatch them at home
  • The powerpoints should emphasize what’s important to know and what is only there to “spark our interest”
  • The biochemistry curriculum involves much unnecessary knowledge
  • The biochemistry and physiology MRTs are useless
  • The physiology practices are mostly useless and should be replaced with seminars

Running a website is not free

Last updated on January 31, 2019 at 18:26

When you run a website must you pay for both the server itself and for the domain name you’re using, which in my case is “greek.doctor”. This server is very cheap, however the domain name costs 89,60 USD every year. If you’d like to help me with this amount would I be very grateful! If you don’t want to that’s fine too.

Here is proof of the amount:

Here is the link to the GoFundMe: https://www.gofundme.com/help-me-pay-for-the-domain-name-greekdoctor

Edit: Thank you all of those who have helped! You gave more than I asked for even though that wasn’t my intention. That’ll pay the server expenses as well.

Shoutout to Sofia, Gowthami, Milica, Èmma, Karl Martin, Silje, Jakob, Ali, Andreas and Daniel (and the two anonymous people) for donating <3 love you

Update regarding the website

Password-protected images

Some images are supplied by the departments at the university with the intention that they should only be shared among students. Because of this will I from now on password-protect these images. At the time of writing does it just include pictures of preparations and histopathology slides in pathology 1, and I’ll definitely do the same for pathology 2. This password-protection may extend to other subjects later, or I might even remove it if it turns out that the department doesn’t mind.

Why do I lock just the images? I believe knowledge should be freely available, so locking just the images with a password and keeping the text available makes more sense than locking the whole website with a password or any other solution.

There is only one password for the whole website. After entering it once will your browser remember the password for 30 days, after which you must enter it again. If you enter the password into one page will all other pages be unlocked, so you don’t have to unlock every single page.

If you’re a student at POTE can you send me an e-mail to get the password. I’ll also post it on Jodel so local students can find it easily. If you receive the password then please share it with fellow students. I apologize for the inconvenience caused by this, but I hope that it will come to a time where the password is spread by word of mouth so the process isn’t so inconvenient. I can see that by the time I applied the passord to the time of writing this (around one hour) has the password already been spread to some extent, which is great.

If you immediately recognize the origin of the password are you a star in my eyes!

Statistics

I thought people might be interested in seeing some website statistics for greek.doctor, so here goes.

There have been 9500 visitors since the exam period started December 10th. That’s an average of 250 students every day. The number of daily visitors was high from the 10th until the 21st, when number was 150-200 visitors per day. Good to see that people took some time off for Christmas despite it being in the middle of the exam period. January 2nd was the average back up to around 300, where it has stayed since.

During the same time period have there been 122 000 page hits, meaning that the average visitor only visits 12 pages, however I think this number is actually higher than that because I suspect that many “visitors” are just robots that only visit one page and not actual students.

There have been 22 500 visitors and 214 000 page visits since I started measuring statistics in June 2018.

The record for most pages visited by one person in a day is 278. On December 13th did one student in Hungary visit 278 pages on greek.

The day with fewest visitors is December 22th, closely followed by December 23rd. 151 and 185 visitors visited those two days, respectively.

The vast majority of visitors are in Hungary, but there is a considerable amount of visitors from USA, Germany and Norway as well, in that order.

The most popular subject by far is pathology 1.

There are 405 different pages in total. That’s a lot!

There are around 20-30 people every day that reach greek.doctor by search engines, mostly from Google but some also from Bing.

Most people that are referred to greek.doctor come from Google. In second place do we have Facebook, which is probably because people send each other links on Facebook messenger. Funnily enough are there also some referrals from Instagram, meaning that people either share links via Instagram chat or people actually click the link I have in my Instagram profile, which is flattering.

Lastly, if anyone have any privacy concerns: I have no way of identifying who visits the website. I can’t even see your IP address. The only information I can see from visitors is:

  • How much time you spend here
  • Which pages you view
  • Which browser you use
  • Which operating system you use
  • Which country you are browsing from
  • How you were referred here (i.e. I can see that many are referred here from Facebook)
  • If you googled something to end up here can I see what your search word was.

Some thanks

I want to thank Sofia Akhtari (username “ms. worldwide”) for helping me write many of the theoretical topics in pathology 1 and pathophysiology 1. It really helped me a lot because there really is a lot to write!

I’d also like to thank all of you who comment to help me find inaccuracies and things I’ve gotten wrong and to improve the notes. Many people, but anonymous and pseudo-anonymous (looking at you, Johannes) have left many comments with improvements, and we’ve had some discussions as well. I really appreciate it!

What’s next?

I’m done for this exam period. Without making any promises or legally binding contracts can I say that I will try to write physiology 1 notes. They definitely won’t be finished before this exam period finishes, but hopefully will they be finished before the physiology 2 exam this spring, or possibly before the next autumn exam period. Don’t rely on it however, as I might not have time to complete them.

We’ll definitely write pathology 2, pathophysiology 2 and pharma 2 for the next semester. I probably won’t have time to write anything else.

If you still have exams left, good luck on them! If you’re already done, enjoy the vacation!