greek.doctor

Please help my friend Anna for her thesis by answering this questionnaire: https://docs.google.com/forms/u/0/d/e/1FAIpQLSdisols-oZ-98UFt_nG56RHz8BuHRMkUs2cFe77nnsB5FJQvA/viewform?usp=send_form&pli=1

It takes 10-20 minutes to complete. Thank you!

A professor at the university of Pécs is conducting a countrywide study, investigating international medical students’ well-being and mental health. The survey is accredited and anonymous.

They have asked for my help in bringing this survey to medical students in Hungary. Please take 12-18 minutes of your time to fill out this survey:

https://forms.gle/dmuv2kVZNjMJrteu9

Spoiler alert: It’s not good.

I’ve spent way too much time writing 21 pages about my experience with the medical university of Pécs, intended to give potential students a look into the life of a student at POTE. You’ll find it in the sidebar.

I also want other students to be able to share their opinion about the university with potential students here. The only thing I require of you is to answer the simple question of “would you recommend this university to a friend or not”. Other than that, you can write whatever you want. Both positive and negative experiences are welcome of course. If you want do to so, message me (email or messenger) with what you want posted and whether you want to be anonymous or not.

via GIPHY

The oral state exam. The last ever exam at medical school.

It’s not known to be difficult; in fact, it’s known to be more of a formality. Virtually no one fail, and people get good grades despite being unable to answer many of their questions.

Even knowing this, the days before the exams were tough. I wasn’t afraid that I wouldn’t pass, but I was still very stressed. I can’t recall the last time I actually couldn’t eat for days due to stress. But hopefully this was the last time.

How it works

On the day of the written state exam (May 25th for us), all 6th year students receive a schedule for the oral state exam, showing you which day you’ll have the exam on. It’s mostly in alphabetical order, and mine was to be June 1st.

On your designated day of oral state exam, at 7:30 in the morning, a Teams group call begins with officials from the university and all the students who are to have their exams that day. There, the officials randomly draw which department each student is to have their exam at. The students must show up at that department at 8:45, and the exam begins at 9.

At 9 you will get a patient to examine. In some departments, mostly ob/gyn and psych, you’re only to take the patient history and not do any physical examination. Following this, there is a practical part where an examiner asks you questions regarding the case and asks you to show certain examinations. This differs a bit from department to department, as some departments combine this “practical examination” with the theoretical examination which comes next.

The next is the theoretical examination. In each department 4 – 5 examiners from different departments/specialities form a board which will examine you. Some of these examiners may be from other medical universities in Hungary. They’ll ask you a few questions from their own specialities, and often look at your thesis and ask you a few questions about it as well.

Some departments won’t give you your grade until everyone has finished their theoretical examination that day, while some give it right away. After you get your grade (and a small rite of passage from the examiners), you’re free of the tyranny!

My state exam

The uni officials drew psychiatry department for me. I went there at 8:30. At 9 I get a patient. Many patients at the psychiatry clinic speak English, so students having their exams there usually get an English-speaking patient. Initially, they told me that there were no available English-speaking patients, and that I would have to get one who only speaks Hungarian, but that a resident would help me out, but when I got my patient, they did speak English, so I was glad. We sat down and had a nice chat for some time as I tried to take their medical history.

After I was finished, the resident comes and talks to me about the patient (not to examine me). She shows me the patient’s chart and medication list, explains their findings, and answers my questions about the patient. Then, there was nothing to do but wait for the board.

I was the second to last student to enter the room. The board consisted of prof Tamás Tenyi from psych, prof András Tárnok from paeds, prof Imre Szabó from internal medicine gastroenterology, and prof András Papp from general surgery. They ask for my thesis (but not my ID or skillbook, neither of which I didn’t have to show), and they start skimming it while prof Tenyi asks me to talk about the patient.

My patient had psychotic symptoms, so after I was done presenting the patient, he starts asking questions related to this.

• Tenyi: What is the definition of psychosis?
• Me: It’s when a person loses contact with reality, and their ability of reality testing.
• T: Yes. What are the symptoms of psychosis?
• M: Delusions and hallucinations.
• T: Yes. And?
• I thought those were the only two. I try to think of something, but can’t.
• T: It’s typical in elderly patients.
• M: Delusions of poverty, that they’re being robbed?
• T: Yes but you said delusion already. It’s something different.
• M: Then I don’t know.
• T: What is it called when an elderly patient doesn’t know where they are?
• M: Disorientation.
• T: And is disorientation a symptom of psychosis?
• In my mind, disorientation is unrelated to psychosis
• M: No.
• T: Yes it is. If a patient is in Pécs but thinks they’re in Budapest, they’ve lost contact with reality, so it is psychosis. Right?
• In retrospect I should’ve guessed that the answer was yes based on where this was going.
• M: Yes, makes sense.
• T: Okay. Tell me the eating disorders.
• M: Anorexia nervosa, bulimia nervosa, orthorexia nervosa, and inverse anorexia nervosa.
• T: What are the subtypes of anorexia nervosa?
• M: Binging purging type, and …
• I couldn’t remember the other type
• T: Okay. What are the symptoms of bulimia nervosa?
• M: Binge eating followed by purging, Russel sign on the knuckles, and weight …
• I pause as I suddenly forget whether bulimia patients are low, normal, or high weight
• M: … disturbance
• T: Okay. What is it called when someone is obsessed with healthy eating to the point where they develop malnutrition?
• M: Inverse anorexia nervosa. I mixed them up
• T: No, that’s something else. You said it earlier.
• M: Oh, it’s orthorexia nervosa.
• T: Yes. So what is inverse anorexia nervosa?
• M: It’s when a person like a bodybuilder thinks that they’re small.
• T: Yes. What are the similarities between regular anorexia nervosa and inverse anorexia nervosa?
• M: Both patients cannot see themselves for what they really are. What they see in the mirror is not the truth.
• T: And what is this called?
• M: Body dysmorphia?
• T: No, body image.
• What?
• T: Okay. What is delirium?
• M: Delirium is an acute decline in sensorium and awareness of the environment caused by somatic disease.
• T: Yes. What are the most common causes of delirium?
• M: There can be many causes. Fever, surgery, cancer, infection, metabolic disorders…
• T: Which are the most common metabolic disorders?
• M: Electrolyte disturbances, and-
• T: Which are the electrolyte disturbances most commonly causing delirium?
• I’d never considered this, but the answer is always sodium, right?
• M: Sodium disturbance?
• T: Up or down?
• M: Hyponatraemia.
• T: Yes. What else.
• What else indeed?
• M: Potassium?
• T: No.
• M: Calcium?
• T: No. It’s not an electrolyte.
• M: Oh. Hyperglycaemia?
• T: Can be, but it’s not common.
• I try to think of other metabolic causes, but I’m drawing a blank.

Sometime around this point in time, I realise that there is a lot of tension in the room. Everyone is just staring at me, not smiling, while I mostly look at the floor. A friend of mine had the exam earlier that day with the same board, and he talked about how chill the atmosphere was and how everyone was laughing. When I realised that my exam had a totally different atmosphere, I start to get a bit anxious. Was there tension because I was doing poorly? Or do they not like me?

• Tenyi: Think about an elderly patient who is okay in the morning but in the evening they have delirium.
• That did not help me at all
• T: Think about heart disease, lung disease, …
• Still no clue
• T: … anaemia, …
• M: Hypoxia?
• T: Yes!
• He lets out a small sigh of relief.
• T: Okay, which other metabolic disorders. It’s something you always check in routine labs.
• I try to picture routine labs in my mind
• T: Think about the kidney, liver …
• M: Oh, of course. Liver and kidney failure.
• T: Yes. What is liver failure called?
• M: Cirrhosis?
• T: Yes, but what is the name of the condition when a patient with liver failure develops neurological and psychiatric symptoms?
• M: Oh, hepatic encephalopathy.
• T: Yes. Do you know the name of the tremor?
• M: Flapping tremor
• I made a small flapping motion with my hand as I said it, as if my words weren’t enough to convince them that I knew the answer
• T: Yes. And what is it called for kidney failure?
• I didn’t know what he was after, but I saw an opportunity for a bad joke
• M: Renal encephalopathy?
• They chuckle a bit
• T: No, it’s uraemia.
• Duh.

I think that was the questions I got from psych. He says that he’s finished, and gives the word to prof. Tárnok. He introduces himself, and says that he finds my thesis very interesting as he’s an expert on IBD.

• Tárnok: Do you know what kind of doctor you want to be?
• Me: I’d like to go into internal medicine, probably nephrology or cardiology.
• T: Not gastroenterology?
• M: No, I find nephrology and cardiology more interesting.
• T: Okay, that’s a shame. And may I ask where you’re from?
• M: I’m from Norway.
• T: I looked through your thesis, and it looks very interesting. During researching for your thesis, did you come across the IBSEN study?
• I pretend to think for a bit, but I’m pretty sure that’s not familiar to me
• M: No, I haven’t heard of it.
• T: It is a famous study on IBD which was made in Norway. Anyway. Could you tell me some differences between IBD in childhood and adulthood?
• This is something I’d never really considered. The only difference I could think of at the time was something I’d read while researching for my thesis
• M: Well I know that in children total enteral nutrition is used to induce remission in Crohn disease, but this is not used in adults.
• T: Okay, that is true, but what about the clinical features?
• M: I don’t know
• I don’t remember if he gave me the answer or if he just moved on to the next question
• T: Which is worse, IBD onset in childhood or adulthood?
• I don’t know why, but for some reason I felt that the counterintuitive answer was more correct
• M: In adulthood?
• T: No, childhood IBD is worse. The earlier the onset, the worse the disease.
• I clearly remember that everyone paused at this point, and this awkward moment was perfect to fuel my already high anxiety
• T: Can you tell me a bit about the treatment of Crohn disease in childhood?
• Finally, something I feel like I know
• M: In children we can use either total enteral nutrition or steroids to induce remission, and we can use immunosuppressants like azathioprine or biologics like adalimumab and infliximab to maintain remission
• T: Can we use biological drugs to induce remission?
• M: No, they’re used for maintenance of remission.
• T: That’s not true, they can be used for induction as well. Can you please tell me which drugs for induction of remission induce mucosal healing?
• While studying CD I’ve never heard the term mucosal healing, so I had no idea
• M: Steroids?
• T: No, the biological drugs. Steroids treat the clinical disease but do not induce mucosal healing, while biological drugs do both. Could you explain to me what step up and top down therapy is?
• M: Step up is when you begin with the least intensive treatment and gradually increase it, while top down is the opposite.
• T: Yes, and which do you use in Norway?
• M: Uhm.. I don’t know.
• T: Okay, do you know who decides whether the patient gets step up or top down therapy?
• M: The treating physician?
• T: No, it’s actually the economists. Top down is more effective but is also more expensive, as biological therapy is more expensive. But, it may pay off in the long run due to better outcomes, so these economists must decide whether the initial increased price is compensated by better outcomes in the long run.
• I don’t recall his answer exactly, but it was something like this. Definitely was an unexpected question, at least.

I think he had more questions, but I can’t recall them anymore. Eventually he gives the word to prof. Szabó.

• Szabó: We’ve been talking about IBD so far, which can increase the risk for colorectal cancer. Can you give me some hereditary syndromes which increase the risk for colorectal cancer?
• Me: Gardner syndrome and familial adenomatous polyposis.
• Sz: Yes, and there is one more.
• I try to think, but I can’t recall
• Sz: It’s a non-polyposis syndrome
• I didn’t realise how big of a hint this actually was when he said it
• Sz: It’s hereditary non-polyposis colorectal cancer. Do you know the gene which is mutated in this syndrome?
• I don’t recall, but I do remember some genes involved in CRC.
• M: APC?
• Sz: No.
• M: P53?
• Sz: No.
• Well, those were the ones I could think of initially. But after thinking a bit, I recall something else which is worth guessing
• M: Microsatellite instability?
• Sz: *visibly surprised* Yes, MLH1 or MSH2, for example.

He gives the word to the final member of the board, prof. Papp.

• Papp: I only have one question for you. Could you tell me the differences in surgical treatment for Crohn’s disease and ulcerative colitis?
• Me: So in UC, surgery can be curative, as it only affects the large bowel, and one can remove all of it, but in CD, surgery can never be curative, as the disease will always recur in the areas next to the excised lesion.
• P: Well yes, that’s true, but what I was thinking of was that in CD you only remove the diseased segment of the bowel, while in UC you remove the healthy part as well.

And that was the last question. Before I leave, prof. Tárnok asks whether I’m certain that I don’t want to be a gastroenterologist. Before I can answer, prof. Papp says (in a joking, non-malicious way) “no, it’s too difficult for him”, after which everyone laughed a bit. It may sound rude, but I could tell that he didn’t mean it in a rude way. The fact that everyone laughed made me feel a bit better.

I think I was in for 20 – 25 minutes. In most cases, no one gets their grade until everyone has had their theoretical part, and that was the case for my group as well. Luckily, I was the second to last student, so I only had to wait for one student to finish to get to know my grade.

I felt pretty shit before the exam, but I actually felt even more shit after it. I knew that they don’t fail anyone, but I felt like I answered wrongly on almost every question they had, and I had an unshakeable feeling that I’d failed.

After the last student finishes, they call all the students back into the room where we had the exam. Prof. Tenyi opens with a small “rite of passage” where he says that from this day on, we’re no longer students, but that the medical profession requires regular studying to stay up to date, etc etc. This made me feel pretty secure that I’d passed, but he follows it up with “however, the performances have not been equal” or something like that. He starts by reading the grades of everyone in the order they had the exam.

As soon as they say my name and “five”, I immediately burst into tears, in front of everyone. Like, proper ugly crying. The relief was immeasurable. Luckily I was the second to last student, so I only cried while they were reading the result of one more student. As soon as they finish and congratulate everyone, I turn to hug and cry in a friend of mine’s arms who also had the exam that day.

I leave the room, and outside some of my closest and bestest friends are waiting for me with lots of beautiful flowers and bouquets, and so my crying reinforces as the tears are no longer just tears of tiredness and relief, but from being super touched as well. They see me ugly crying and assume the worst (understandably), but I tell them I got a 5, and they become a bit confused as to why I’m crying so much. While outside, still crying, prof. T´´arnok comes over to shake my hand and congratulate me. Just a bit awkward.

Parting words

A select few graduating students had experiences like me, where they were in for a long time and got asked some difficult questions. The vast majority had really simple, 5 – 10 minute exams with baby questions. But, the most important thing is that, no matter which of these two group you end up belonging to, you’ll pass. The oral state exam is not an exame where anyone fails, but it’s still a source of severe anxiety for many, as it’s the last of the last, and failing it would be devestating. Personally, I was super nervous and lost my appetite for almost a whole week before the exam, and it took some days after the exam for these feelings to disappear. Honestly, by having a terrible oral state exam experience, you’ll leave the university with a proper POTE exam as your last exam experience, which is kind of poetic. Full circle.

In the two weeks since the exam, the graduating students have celebrated, by dancing in a public fountain to the music of a live band (a POTE tradition), by going on a trip to lake Balaton, and by partying a lot. We’ve also rested, for the first time in 6+ years without any school-related worries. Even 2 weeks after finishing, we still have moments of realisation, where we realise that we’re actually actually finished. Our Neptun now shows our student status as “Graduated”. From now on, the adult life starts, and a big chapter of our lives is completed, for good and bad.

I’ll write a post later with what’s next for the website. Even though I’m finished, I still have plans to improve and maintain it, and I’ll definitely not take it down, as many have been worried about.

Congratulations to the graduating class of 2022!

The written state exam is May 25th. For those who are unaware, this exam consists of 180 multiple choice questions in 150 minutes, and all the questions are provided upfront on the website finalexam.hu. However, the website only allows viewing 20 questions at a time. Questions may change every year, and so documents from previous years containing all questions are likely not very useful. As such, it’s beneficial to find a method of collecting all questions into a document. Copying and pasting manually takes a lot of time, so I tried to come up with a better solution.

I don’t have a lot of experience with programming, but I knew that I know enough to program a script which automated the process. After a few days of working on it, it’s finished. The repository for the source code is here, and the code will likely continue to work in the future, and so can probably be reused in the future.

I’ve uploaded the document with all the questions to the facebook group for 6th year.

Next, I’ll try to automate the process of converting the questions to flashcards.

Edit: Flashcard conversion is done. The repository is here, and the flashcards have been uploaded to the facebook group.

Edit2: The link to the 2022 state exam questions anki is here. Note that questions may change from year to year, so it would be best if someone remade the anki every year using the tools I made (or with self-made tools).

So I had my internal medicine final at 1st department on the 21st. A notice on Neptun told us to meet at the “Clinical and Educational office” in the B wing of the 2nd floor (room B227) at 8:00, and to bring our 8 case reports and certificate of finishing the practice. When we arrived, they took photocopies of the case reports and certificate, and gave us a paper which we were to bring to the practical part of the exam. We were told to wait outside, and eventually prof. Gabriella Pár comes and gets us and gives a patient each. We were two students per room, each with their separate patient. She tells us that she’ll be back to ask what we’d found in 30 minutes.

Practical part

I introduce myself to the patient and begin taking the anamnesis and performing the physical examination. After me and the other student finish with each of our patients, we leave the room and wait for the professor in the hallway while we collect our thoughts on the patient. While waiting, my patient comes out of the room and offers both of us some tea ❤️.

Eventually, after maybe an hour, the professor arrives. She asks me what I’d found, and I begin presenting my findings. My patient had arrived to the hospital due to abdominal pain which occured after eating. She stops me and begins asking questions.

• Examiner: What can cause abdominal pain after eating?
• Me: For example gallstones and gastric ulcer.
• E: Yes. In case of duodenal ulcer, when does the patient have pain?
• M: At night
• E: Yes, and two-three hours after eating. What else can cause abdominal pain after eating?
• M: Acute pancreatitis.
• E: Yes. In case of gallstones, where does the pain radiate?
• M: To the shoulder (thanks to my fellow student who just told me this before my exam, otherwise I might’ve not remembered)
• E: Which shoulder?
• M: The right shoulder (I had to think for an embarrassingly long time to recall which side the gallbladder is on)
• E: And in case of acute pancreatitis?
• M: It radiates to the back.
• E: Why does the pain in acute pancreatitis radiate to the back?
• M: Because they share the same nerve supply? (I don’t remember what I said but it was something vague like this)
• E: Something like that. What are the risk factors for gallstone?
• M: It’s the six F’s: female, forty, fat, fair-skinned, fertile, …, and I can’t recall the last one
• E: Does your patient have any risk factors for gallstones?
• M: He’s fair-skinned and overweight.
• E: Anything else?
• M: (thinking but can’t recall anything)
• E: What are the types of gallstone?
• M: Cholesterol and pigment stone… oh, so dyslipidaemia is a risk factor.
• E: Yes. How can you tell that your patient has dyslipidaemia?
• M: (I couldn’t see any xanthomas or xantholasmas, so I don’t know)
• E: It’s a question you asked your patient.
• M: (What question could I possibly have asked to determine that)
• She looks at the paper in which I’ve noted my patient findings and points at the medicine list.
• M: I could ask if my patient takes statins?
• E: Yes, exactly. Does your patient take statins?
• M: I’m not sure. He told me that he takes heart medicine but I didn’t ask more specifically. He wanted to show me the list of medications but he couldn’t find it.
• E: It’s okay. What other question you asked could show that he has dyslipidaemia?
• I look back down at the paper
• M: He had a myocardial infarction in the past
• E: Yes, exactly. What side effects can statins have?
• M: It can cause myopathy or liver failure, for example.
• E: What is myopathy?
• M: Inflammation of the muscle which can cause muscle weakness and pain.
• E: And what abnormality can you see on the labs?
• M: Elevation of creatinine kinase.
• E: Yes. What can be a complication of rhabdomyolysis?
• M: It can cause kidney failure.
• E: Good. How much alcohol does your patient drink?
• M: He said he drinks only a little, but I don’t know how to ask more specifically.
• E: Okay. What’s the daily limit of alcohol intake?

This is something I wouldn’t have learned unless a friend of mine had gotten the same question and warned me about it, so I looked it up in the lecture.

• M: It’s 20 – 30 g for men and 10 – 20 g for women.
• E: Yes. How much alcohol is there in one beer?

I’ve always thought that one beer was one unit, and I’m pretty sure it said on the lecture that one unit is 10 g.

• M: It’s 10 g.
• E: No, that’s not correct.
• M: But it depends on the strength and size of the beer, right?
• E: Okay, how much alcohol is there in 1 dl of regular beer?
• M: 3g? (pure guess)
• E: No, it’s 4 – 5g. So how much in halv a litre?
• M: 20 – 25g.
• E: Yes, so one beer is already above the limit for women and above the limit for men. Please show me examination of the liver.

I percuss the border of the liver.

• M: His liver is 1 finger below the costal arch.
• E: Okay. What can cause the dull sound over the liver to disappear?

That’s a problem I’d never considered or heard of before, but I figured that the only way it can disappear is if air gets between the abdominal wall and the liver.

• M: If there is air in the abdomen?
• E: Yes. How can you diagnose air in the abdomen?
• M: You could use x-ray or CT.
• E: How would you see abdominal air on x-ray?
• M: There would be air under the diaphragm.
• E: When the patient is in which position?
• M: When they are standing.
• E: And if they are lying down?
• M: Then it would be beneath the abdominal wall?
• E: Yes. What can cause abdominal air?
• M: A perforation
• E: Perforation of what?
• M: The gastrointestinal tract.
• E: Yes. What is the treatment for GI perforation?

I was kind of confused, because I know of no internal medicine-related treatment of GI perforation. Could there be an endoscopic procedure? No, there can’t be. It has to be…

• M: Surgery?
• E: Yes. So it’s a surgical problem and not an internal medicine problem.

And that was the last of the question on the practical part. She writes a 5 on the paper from earlier, and signs and stamps it (of course). She tells me that my examiner will be prof. Alizadeh and that the theoretical part will take part in the science building in room B001, and that he’s impatient and that I have to hurry there, so I thank my patient and rush over there.

Theoretical part

After rushing over there, I found like 10 students waiting outside the room. They’d also been told to hurry, just to have to wait when they got there. One person already finished their theoretical exam but didn’t get their grade because the examiners had told them that no one will get their grades until all 11 students have finished their theoretical examination. So I sit down to wait. After the 9 students before me have finished, it’s my turn. I go into the room, sit down in front of prof. Alizadeh of haematology and (I think) prof. Tótsimon of cardiology. In my fluster I tell them “good afternoon” even though it was like 10:30. As I sit down, Alizadeh leaves the room, presumably to go to the toilet. Prof. Tótsimon begins the questioning in his absence.

• Examiner: Tell me about anticoagulants. Which types do you know?
• M: You have the vitamin K antagonists like warfarin or dicoumarol, the DOACs like dabigatran and apixaban, and the heparins, both unfractionated and LMWH.
• E: Good. In which cases do we use anticoagulants?
• M: Anticoagulants are used in case of atrial fibrillation to prevent stroke, in DVT/PE, and in acute myocardial infarction.
• E: Good. There’s one more.

I try to think but I can’t recall it.

• E: It’s also used in nephrotic syndrome, but it’s okay if you don’t know. (I actually did know but I’d never thought of that in a million years)
• E: When do we use vitamin K antagonists and when do we use DOACs?
• M: Generally, VKAs are only indicated in case of prosthetic heart valves or in case of moderate or severe mitral stenosis.
• E: Good. In which case of atrial fibrillation do we use anticoagulation?
• M: If the CHA2DS2-VASc score is 1 in men or 2 in women.
• E: Actually in case of 1 for men or 2 for women, anticoagulation can be considered, but if it’s 2 in men or 3 in women, then it’s recommended. But it’s good, your answer is good. Do you remember the parameters of the CHA2DS2-VASc score?

This is something I imagined could be a question, so I’d prepared for it. I close my eyes and try to visualise the mnemonic. To my own surprise, I recite it correctly.

At this point prof. Alizadeh returns to the room. Prof Tótsimon quickly explains him in Hungarian what we’ve talked about so far. Prof. Alizadeh continues:

• E: So my colleague tells me that you’ve talked about anticoagulants and that you’ve answered excellently so far. Now, please tell me. What are the antidotes for DOACs?

I was not prepared for such a pharma question. I remember studying it in pharma but I hadn’t looked at it since. We spend some time in silence as I try to dig deep into my memory for the information, but I can’t recall it.

• E: Okay then please tell me, what are different types of DOACs?
• M: You have dabigatran, which inhibits factor II and X, and the others like apixaban and rivaroxaban, which inhibit only factor X.
• E: Dabigatran inhibits only factor II, but yes. Now, each of these groups have different antidotes. Please tell me what they are. The antidote for dabigatran begins with an “I”.

The hint made some gears turn in my head.

• M: Is it something like idarocumab? (I don’t recall exactly what I said, but it was something like this, which was not very close to the correct name)
• E: Yes, it’s idarucizumab. The antidote for the others are andexanet alpha and ciraparantag. Now, for a better grade, please tell me the newest drug for atherosclerotic ischaemic heart disease.

At first, I’m like, what. I’m pretty up to date on cardiology, but I can’t recall any new drugs for that indication. I know that SGLT2 inhibitors were recently indicated for heart failure as well. Could that be what he meant? But that’s not related to atherosclerosis.

• E: It’s four letters and a number. It’s an injectable drug.

Okay, but then it has to be them, right?

• M: SGLT2 inhibitors?
• E: No, that’s for heart failure.

I knew it.

For the next part, I believe they gave me a hint which put me on the right track to the answer, but I can’t recall what the hint was. It might’ve been the first letter, “P”.

• M: It’s PGSL2 inhibitors, or something (I don’t recall exactly what I said, but it was nowhere close to the correct answer lol)
• E: Yes, it’s PCSK9 inhibitors. It’s okay, please go out and wait for your grade.

Epilogue

After waiting for the 11th student to finish their exam, everyone went back into the room one at a time to get their grades. As I enter when it’s my turn, the examiners are already on their way out, so I think they kind of forget about me. As they walk past me, they tell me that I got “excellent” and congratulated me.

And that was it! That was my last ever exam at POTE. Now only state exams remain. I was surprised to be asked such an amount of pharma questions, but anyway.

So I had my neurology final yesterday. The exam was to begin at 10:30 (which sucks, I prefer having early exams). I was waiting outside the neurology department (one floor up from psychiatry) with the other students. According to Neptun, our examiner was to be prof. Janszky.

It’s 10:30. A doctor comes and guides us to the department’s “library”, quotation marks because there were zero books in there..

Practical part

She asks who of us had reflex hammers, which only I and a few other students had brought (but I’d forgotten my lab coat, so we were even). Those of us who had forgotten to bring lab coats were given disposable isolation gowns, and those who’d forgotten to bring a reflex hammer were either lent one or told to borrow from those who had one.

It’s 10:46. The doctor gives each of us a patient to examine, and tells us that we should perform a full neurological examination, and after 20 minutes, she’d return and ask what we’d found and ask a few questions.

So we do the examinations on our patients, and then we wait. The wait turns out to be more like one hour. (She had to examine four students before me, which is why it took so long.)

When she finally returns, it’s 11:38. She begins by asking me what I’d found. She then asks a few theoretical questions:

• What is intention tremor?
• Where can the lesion be if there is an intention tremor?
• How do you examine the muscle tone?
• What is rigidity and what is spasticity?
• If there is a lesion in the pyramidal tract, what kind of muscle tone can be present?
• Demonstrate Hoffman and Trömner sign
• What is the other major pyramidal sign and how do you examine it?
• What are the signs of peripheral paresis?
• Demonstrate on the patient how you would examine the visual field.
• What’s hemianopia?
• Let’s say that I had a stroke in my right hemisphere. What kind of visual field disturbance could I experience?

And that was it for the practical part. I didn’t answer all questions perfectly, but more or less, so I got 5 in the end. It took five minutes.

Theoretical part

She tells me to go back to the library to draw topics. It’s 11:45, lunch time. I draw my three topics:

• A/9: Muscle biopsy
• B/29: Myasthenia gravis
• C/22: Treatment of traumatic brain injuries

My B topic was great, C was okay, and A was not the best. I sit down to write my topics, but there are three students before me, plus the student who was currently having the exam. I knew it was going to be a long day, but I hadn’t brought food.

Time passes, but feels like it’s standing still. Each student’s exam takes like 20 minutes. The exam is happening in another room, so we have no idea how it’s going with the examinees. Hunger grows stronger and stronger. I look at the other students, and they ask me what the time is, as I had my watch. “12:30”, I say, and one student rubs their belly to signal that they’re really hungry. I know, I know. I am too.

I’m hungry, restless, and anxious as we’re sitting there waiting. Nothing is happening in the room; everyone’s is just waiting. The doctor watching over us is droodling on a piece of paper. I look outside the window, hoping to find something interesting to look at to pass the time, but the view consists of an opposing wall with flaking paint. My akathisia is getting to strong; I have to move. I get up and start walking back and fourth in the room. My watch counts 1149 steps as I keep walking to pass the time and ease my anxiety.

Finally, the last student before me returns from her exam. I look at my watch; it’s now 13:03. She walks me to prof. Janszky’s office. A nice office. The doctor who examined my practical part is present as the co-examiner. I sit down in a comfy chair, and he tell me that I can start with whichever topic I would like. Nice.

B/29 Myasthenia gravis

I began by mentioning everything I’d written down, except the part about Lambert-Eaton. I wasn’t sure if I should mention the treatment, but I did anyway and he didn’t correct me or stop me.

He asks me whether there are any other antibodies associated with MG. I forget about anti-MuSK so I mention the anti-VDCC antibodies, but he replies that they’re associated with Lambert-Eaton and not MG. I draw a complete blank on the anti-MuSK. After a while, he gives me the answer, and tells me to go to the next topic.

C/22 Treatment of traumatic brain injury

I begin with who needs a CT and who don’t. It’s probably not actually a part of the topic, but I found it interesting so I wanted to include it anyway. I open with “So I’m Norwegian, so I’ve looked at the Scandinavian guidelines” they laugh a bit and say something like “maybe they’re better”.

After explaining that, I begin by talking about how we only can treat secondary injuries and not primary, etc. etc. At some point he stops me to ask about the types of TBI. He begins with commotion (which I think is a Hungarian term for concussion), and asks me to list the others. I explain contusion, ICH, SAH, SDH, and EDH, and say that if there’s a haematoma we can drain it and if there’s bleeding in the intraventricular space, we can use a shunt. He agrees. Afterward I continue with the supportive treatments I’d listed for oedema, vasospasm, etc.

He asks me what the lucid interval is, and I answer. He asks me why we examine the eyes in TBI, and I say it’s because anisocoria could be present. He asks why anisocoria occurs, and I say herniation of the cerebral peduncles, to which he replies that it’s wrong, it’s rather uncal herniation. “In case of anisocoria, which pupil is on the side of the injury?”, to which I reply “the larger pupil”. He agrees.

He asks what another finding may be on the eyes in case of TBI. “Fixed pupil, when there’s no reaction to light”, I respond. He asks which nerve is affected in this case, and I say occulomotor. He signals for me to proceed to the last topic.

A/9 Muscle biopsy

I begin by listing what I’d written down. I don’t get further than the IBM point until he interrupts me and tells me that we’re finished and that it’s a 5. Yay! The exam took 7 – 8 minutes.

On my way out, they ask me for the three envelopes each of my topics were inside when I drew them. I had forgotten them in the library, so I had to go and get them. Awkward!

I look at my watch. It’s 13:13.

Time for lunch.

My thesis defence was March 11th. My thesis topic was “Diet in Crohn disease – The effect of diet on the microbiome and its role as a therapeutic modality”. You can read it here. The thesis defence involves defending your thesis against a defence committee consisting of three people, two of which are your designated opponents.

Before the defence

My supervisor was the head of the gastroenterology division of the 1st department of internal medicine, prof. Áron Vincze. Him and dr. Judit Bajor were designated as my two opponents, and as opponents are supposed to do according to the rules, they gave me their separate evaluations of my thesis ahead of the defence.

I was informed of my thesis date by e-mail only 15 days ahead of time, a date they’d chosen without my input. I had already planned a practice in Norway at that date, a practice I had planned 6 months earlier. Plane tickets were already bought. I replied that the date is not appropriate for me, and that we either need to find another date (I had other suggestions which were within the deadline of April 1st) or have it online. The reply was that either of these options would be impossible (even though I know of other students who had it online or were allowed to choose the date themselves). I was also told that the middle of March was the “usual time” during which the 1st department holds its defences, but no one never informed me of this. This means that they were aware of the approximate date of the defence for a long time but decided to inform me only 2 weeks before.

Note that there were no critiques or questions in the opponents’ evaluation. In most cases, students receive questions ahead of time of their defence so they can prepare and answer these questions during the defence. I’d received none.

In most cases, the student is asked to hold a 5 – 10 minute presentation about their thesis during the defence, with or without a PowerPoint presentation. I asked whether I should prepare a pptx, and they replied no, so I assumed I’d have to hold a presentation with no visual help. However, I asked another student who were to have defence with the same department at the same date, and they were told that they shouldn’t have any presentation at all, and that the whole defence should only be reserved for the questions received ahead of time.

So I wasn’t going to hold a presentation, and I hadn’t received any questions. The last days before my defence I was really stressed because I had no idea what I would have to do at the defence. Would I only receive questions for which I couldn’t prepare? Had I received wrong information and would have to hold an impromptu presentation?

Brief summary of my thesis

The gist of it is that there likely exist some possibilities for dietary treatment of Crohn disease, as evidenced mostly by 2 things: Firstly, the well-known efficacy of exclusive enteric nutrition (EEN), the practice of inducing remission in Crohn disease by putting the patient on a nutrition drink-only diet for 6+ weeks, and secondly, the fact that temporarily diverting the faecal stream by using a temporary stoma causes lesions distal to the diversion to heal, and the lesions only recur when the stoma is reversed, which indicates that components in the faeces are important in the development of these lesions. There are a few small studies with special diets for Crohn disease which show some promise, and these diets generally exclude certain food groups (gluten, milk protein, lactose, alcohol) as well as other modifications, but larger studies are needed. As of yet, there is not much evidence to recommend any specific dietary changes in Crohn disease.

The day of the defence

The time of my defence were to be 13:20, so I showed up at approximately 13:00. It turns out that the student who were supposed to start at 13:00 hadn’t started their defence yet, because a member of the defence committee was late, so the whole ordeal was already delayed. While waiting, one member of the defence committee for my defence shows up and waits with us. We have a nice chat, and he tells me that neither of my opponents are present today, so their places on the committee has been replaced by two other doctors. However, according to him, on a defence committee only the opponents have actually read through the thesis, but since both of my opponents were absent that day, none of the members of my defence committee had read through my thesis (although in retrospect I believe one of the members might have read through it on his own initiative, but it’s impossible to know for sure).

He also tells me that I should begin the defence by summarising my thesis in 10 sentences, “of which the first four should be especially good”, and that they’d just ask a few questions and that would be that. I’m glad he told me that, so I at least had a few minutes to mentally prepare some sentences before going in. Eventually, after some delay, it’s my turn.

The defence

They invite me into the library, and ask me to take a seat at the table in front of the three committee members. They are, in no particular order: prof. József Zsimmer, prof. László Czopf, and prof. Imre Szabó. They begin by asking me to briefly summarise the topic of my thesis. I intended to make it 10 sentences but I think it ended up lasting 3 – 4 minutes instead. Some of the questions they followed up with which I remember were:

• What are the main suggestions regarding diet in Crohn disease? (For example exclusion of certain dietary factors like gluten, milk protein, alcohol)
• Do you think that there are any differences between the different stages or extents of the disease regarding these factors in the diet? (Most likely the localisation, severity and type of CD could influence the dietary treatment)
• If there is a patient with fistulising disease and no large bowel affection, what would be your suggestion about the diet? (Here I think I answered that they should avoid dietary fibre, but only because I misheard him so I thought he said stricturing disease, in which case dietary fibre avoidance is correct, but I don’t know what he was going for with this question)
• If you advise dietary restriction to a patient, which by evidence decreases the microbiome diversity, which is potentially harmful, what are the possible correlations with Crohn disease? Are there any evidences or is it too early to talk about? (I think I replied that it’s too early to know, and that during my thesis work I only found evidence of short-term changes in microbiome following dietary modifications in Crohn disease)
• If you analyse a Crohn disease patient for other parallell disorders like food allergies or intolerances, would it change the approach? Do you think these restriction diets work in some cases but not in general because of these comorbidities and not necessarily because of the Crohn disease itself? (I think I answered that yes, that could be a possibility)
• Do you have any data on detailed analysis of the microbiome in Crohn disease patients? (Yes I do, there is a section in my thesis about it. Analysis shows that in general CD patients have less microbiological diversity, lower absolute number of microbes, decreased proportion of “good” gut bacteria and increased proportion of “bad” gut bacteria)
• What is the risk factor if you decrease the microbiome diversity in an autoimmune disease like Crohn disease? Because these restriction diets will decrease the diversity. (I replied that I haven’t seen any studies on whether restriction diets affect the microbiome diversity and whether it has any negative effects on the activity of Crohn disease)
• Do you know of any gastrointestinal diseases which can benefit from modifying the microbiome? (I didn’t know what to answer to this. I only replied small bowel bacterial overgrowth, I think)
• If you would investigate the diet in case of Crohn disease, which approach or direction would seem to be the most feasible for you? (I’m not sure I understood his question correctly, but I think I answered that we could use food questionnaires or asking patients to write down what they eat)
• Do Crohn disease patients have different nutrition than healthy people? (Yes, it’s covered by my thesis that CD patients often avoid foods which they feel make their symptoms worse. They often avoid healthy foods and eat unhealthy foods like soda and snacks)
• Do you consider this to be related to the easier absorption of sugar from these foods? (Yes, that could be an explanation, considering the possibility of malabsorption in CD)

The last line of questioning was the most memorable one:

• Committee member: Based on the results of your thesis, what would be your suggestion to a patient with Crohn disease regarding diet?
• Me: Based on what I’ve read, I’d recommend patients to experiment with their diet, so they could for example exclude one food group from their diet, and—
• C: Based on what? Their relief of symptoms?
• M: Relief of symptoms may be one measure, other could be for example changes in blood tests like CRP level—
• C: Based on CRP you would suggest food diet restriction?
• M: No, just—
• C: This is restriction. If you tell the patient to not eat something, it’s restriction. It can be harmful. You would suggest, without evidence, for the patient to do that?
• M: If they’re interested in trying an approach which is not yet evidence-based, then I would suggest them to restrict certain food groups—
• C: Based on what?
• M: Based on the little evidence that is already present, for example the CD-TREAT diet which I mention in the thesis, which avoids alcohol, lactose-containing milk products and gluten, and these patients have shown good results in inducing remission. So this is—
• C: But that’s not true!
• I’m stunned into silence at this point.
• C: Alcohol okay because it’s harmful, in general we should suggest to avoid it. But you would ask your patient to do a restriction diet, which can be harmful because we know that if you decrease microbiome diversity that’s not a good thing, even without evidence. You should be aware about what you suggest. It can be dangerous. You can not restrict diet if it’s harmful, okay? You can suggest a lot of things, but you’re going to be a medical doctor so you should follow the evidence.

The last line of questioning really took me aback. I don’t know of the evidence that restricting certain food groups can be dangerous like he was talking about, and he obviously wasn’t aware of the studies I was talking about. I suppose vegans, vegetarians, coeliac disease, and lactose intolerance patients worldwide are living dangerously.

Following this, the committee leader thanks me for the presentation and “especially for your work”, which he said he thought was very nice and opens a window into a new area of IBD research. That was very nice of him to say.

Then they started discussing the grade. They check my opponents’ evaluations (both 5), and the leader of the committee suggests 5 as well and asks if the others agree. The member who held the last line of questioning replied that he would give “maximum a 4, maybe even a 3”, but luckily for me the other two members suggested 5 and majority rules. In total, the whole defence took approximately 15 minutes.

And that’s all I have to say about that.

So I had paediatrics final on the 3rd. We got no information on email ahead of the exam, but the time of the exam was 8:30 according to Neptun. I’d heard from other students who had the exam that I should show up at the southernmost part of the main corridor of the main building, close to where the library is. Because I’m an idiot I arrived a bit late, so I wasn’t among the first 3 students to be taken in. After the first student was done with their exam, I entered the room to draw topics and prepare.

The examiner that day was prof. Décsi, and the co-examiner was a young male doctor whose name I don’t know. After each student picked their topics, the professor allowed the co-examiner to choose one of the three topics to examine by himself.

My topics were:

• 15. Disorders of the humoral immune system
• 24. Hepatomegaly. Causes, diagnosis, differential diagnosis
• 15. Most common congenital heart abnormalities not causing cyanosis

The co-examiner chose the hepatomegaly topic to examine me in, and the professor asked me which topic I wanted to start with. I chose the immune system one.

15. Disorders of the humoral immune system

I began by telling him what I’d written down. He then begins asking me questions.

• Examiner: You mentioned the repeated and severe infections as a symptom of these disorders. What other symptoms may draw your intention to a disorder of the immune system?
• Me: So these disorders could also increase the risk of autoimmune diseases
• E: Yes. (But clearly not what he was going for) In a young child what kind of frequently occuring problem may call your attention to a potential immune disorder.
• M: (Not sure) Frequent urinary tract infection?
• E: Yes. (also not what he was going for) And what’s not far from this problem? Which is actually a manifestation of bacterial presence?
• M: Uhm, sepsis?
• E: No, in the end of course but not was I meant.
• M: Pyelonephritis?
• E: Pyelonephritis is also a urinary tract infection. What other tract can be infected and give very specific and easily detected symptoms.
• M: Gastrointestinal infections?
• E: Yes, and what will you see?
• M: Bloody stool. (Was thinking of bacterial gastroenteritis)
• E: Yes but mostly just diarrhoea. Frequent and unexplained diarrhoea. And, if the child has repeated infection and diarrhoea, then what other functions of the child will be disturbed?
• M: Growth?
• E: Oh yes. These are the three major symptoms. Next question: If a child has selective IgA deficiency like you mentioned, the diagnostic of which diseases can be complicated by this?
• M: Oh, well that’s a difficult question.
• E: Oh well yes. Up until now you did well so I increase the complexity of my questions. So where do we use IgA in the diagnosis?
• I was thinking hard on this one. For some reason coeliac disease popped into my mind, but I wasn’t confident enough to say it.
• E: It’s no problem if you can’t answer this.
• I gave it some more thought but couldn’t come up with an answer.
• M: I’m not sure.
• E: It’s coeliac disease. (Damn it! I should trust my gut.) If the patient has IgA deficiency, they will not have high levels of the antibodies we use to diagnose coeliac disease. No problem. Next topic.

15. Most common congenital heart abnormalities not causing cyanosis

Once again I began by telling him what I’d written down about ASD. I start to list symptoms of heart failure as I explain symptomatic ASD, and I mention hepatomegaly, poor growth, dyspnoea, sweating, problems with feeding. He then interrupts me with a question:

• Examiner: What is the first sign of cardiac decompensation, before the symptoms you mentioned.
• Me: Oedema?
• E: Before oedema.
• Thinking
• E: How does the heart try to compensate?
• M: Tachycardia.
• E: Oh yes. Please continue

I continue with VSD and the rest of what I wrote down, and he has no questions after this. I continue with my last topic, at which point I turn to the co-examiner (as this was the topic he chose to examine me on).

24. Hepatomegaly. Causes, diagnosis, differential diagnosis

I begin by listing the possible causes. I then continue like this:

• Me: So in the evaluation of hepatomegaly physical examination is important. In newborns it can be physiological that the liver can be palpated 1 – 2 cm below the costal arch, but in older children you shouldn’t be able to palpate the liver that well. Ultrasound is important in accurate estimation of the size of the liver, but for proper differential diagnosis it’s not enough to only look at the liver, we must look for other features of the disease like jaundice in hepatitis, in mononucleosis you’d have cervical lymphadenopathy, in leukaemia there’d by symptoms of bone marrow failure and splenomegaly. And.. Uhm, yeah, that’s all I had prepared.
• Co-examiner: Okay, so. Hmm. He turns to the professor and says: I think he said everything, I don’t have any questions.
• Examiner: Okay, then let me ask a question. Please give me some special causes of young infant or neonatal hepatomegaly. What is the usual size of the liver at the age of 1 month?
• Oh no, is he expecting a size in centimetres? I don’t know and I’m afraid of guessing because I might be so far off. As I’m thinking about this, he continues:
• E: Is there some difference in the evaluation of liver size below or above one year of age?
• Now this is a common problem of oral exams. I feel like he’s after the fact that the liver can be physiologically palpated in infants, but I already said that in the beginning of the topic. Did he not hear me? Or is he after something else? I’m not sure, but I assume the former.
• M: So, compared to the body size, the liver is larger in infants than in older children.
• E: Yes. Also, the diaphragm is lower. So, during the first year of life, if you palpate the liver 2 cm under the costal arch then it can be physiological.
• I was right, he didn’t catch it when I said it the first time.
• E: Let’s say you have a one month old child with a liver palpateable 4 cm below the costal arch. What might be the cause?
• M: Something like biliary atresia?
• E: Yes, what other features of this biliary atresia can you see or detect during the physical examination?
• M: They would have jaundice.
• E: What type of jaundice?
• I don’t know of multiple types of jaundice, so I assume he means indirect/direct hyperbilirubinaemia?
• M: They would have direct hyperbilirubinaemia.
• E: Yes, and with your eyes, what can you see on the patient? What will be the colour of the skin?
• Now this is kind of a lucky coincidence, because I learned the answer to this exact thing during my paeds practice here in Pécs. Apparently (and allegedly), direct hyperbilirubinaemia causes a more greenish jaundice than the “usual” indirect hyperbilirubinaemia. This isn’t something I’ve heard of anywhere else, and internet search doesn’t reveal more than a few papers about it. However, as he asked this question I was pretty certain that that was the answer he was looking for.
• M: It will be more greenish.
• E: Yes, excellent. It’s a 5.

Conclusion

My exam took about 10 minutes. Neither examiner interrupted me often while I was presenting my topic, and if they did it was usually just to say “yes” or “good” now and then, which was nice. I also think it was nice of the professor to allow the co-examiner to practice examination like this. As they say, it sucks to study for paeds but the exam is quite nice. It was a good experience.

I have my thesis defence on March 11th, and neuro on April 7th. Until then, I’ll be playing Elden ring.

Hei! Så hyggelig at du ville sjekke hva prosjektet mitt innebærer. Artiklene jeg har skrevet er sortert etter fag, som igjen er sortert etter studieår. Hvis du vil se på noen av dem kan du for eksempel ta en titt på artikkelen om antikoagulantia og antitrombotiske midler i farmakologi, artikkelen om O2 og CO2 transport i kroppen i fysiologi, artikkelen om intrauterin veksthemming i fødselsmedisin, artikkelen om akutt appendisitt i kirurgi, eller artikkelen om akutt koronarsykdom i indremedisin. Hvis du har lyst til å se litt statistikk om hvem og hvor mange som besøker nettsiden kan du se på det her.

Med vennlig hilsen Nikolas

PS. For my non-Norwegian-speaking visitors, this post warrants explaination. After finishing medical school as a Norwegian, before applying for residency in a specialisation, one must complete 18 months of medical “internship” in internal medicine, surgery, and general practice, called LIS1. The application period for LIS1 is now, and I mentioned this website on my application, so I figured I’d give all potential employers a proper welcome.

UPDATE: I did not get a spot for LIS1. I’ll have to apply again the next round, which is half a year after the first round.