greek.doctor

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.

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.

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).

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!

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

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

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!

It’s that time again. I had pharma 1 written today.

50 questions, all single choice, true/false, multiple choice, relationship analysis and other shit. The questions are on a powerpoint presentation which is limited to 1 minute per question, and an additional 45 seconds for each question after cycling through all questions once. There is enough time for each question, don’t worry, however it gets very annoying quickly because you always have to wait for the next question.

The written exam starts at 14:00, which they tell you by e-mail the day before the exam. The oral starts at 8:00. We got the result 16:45. I got a 4, if you were wondering.

Now, for the part you came here for:

What should I know for the written exam?

The most important drug classes by far are the cholinergics (topic 14 and 15) and the adrenergics (topic 18 and 19). We got questions about the other drug topics too, so you should definitely shouldn’t skip them.

You should know which receptor subtype acts on what, especially for muscarinic and adrenergic receptors – i.e. which muscarinic controls salivation, which adrenergic activates vasoconstriction, which activates vasodilation, and so on.

You should know the two different mechanisms of treating hypertension – either with drugs that block vasoconstriction via α1 or by blocking positive heart effects via β1.

In my opinion should you spend most of your time understanding what the function of each receptor is – that way is it much easier to imagine what its therapeutic potential is and what possible side-effects could be. Oh, M3 activation causes salivation? M3 blockers must cause dry mouth then, and M3 agonists can treat dry mouth. Oh, α1 activation causes urinary sphincter constriction? Better not use α1-agonists in people who already have problems urinating. That’s how you should learn and think.

You should know which drugs act on which receptor and which subtypes, of course.

We got one question where the duration of action was important – it was a comparison between two beta blockers. I never bothered to learn the duration of action of drugs. I don’t think you’ll get more than a couple of questions about it, max.

You should make flashcards where the front is a disease or condition and the back are the drugs that can treat that condition. We have already made such flashcards and you can find them in the menu if you want to use ours.

They do ask questions from the seminar, so don’t skip it. At least read and know the summaries I made for some of the seminar topics. For the topics I didn’t make summaries – make your own. For us were the most important seminar topics 5, 6 and 13, and I do think those are always the most important, but you should read the others too. They don’t ask very difficult questions about it – if you’ve read through it should you be able to answer just fine. Memorize the formulas for loading dose and maintenance dose.

You should know which drugs can induce myosis and which can induce mydriasis, with and without cycloplegia.

Do the sample test! It’s on neptun with the answer key, and the questions we got were similar, some even almost identical.

Cool

That’s all I have to say about that I guess. I’m almost done – just internal med left on tuesday. I probably won’t write about that experience, unless you really want me to.

Good luck on your exams! Don’t bother asking me for past papers because I don’t have any.

I had Micro 1 yesterday. Since it’s a written exam will this post be different from the previous ones.

Preparation

I used the “Clinical microbiology made ridiculously easy” book for basic theory on bacteria, antibiotics and viruses. I also used Sketchy micro for details on viruses. I didn’t use sketchy for antibiotics, although I’ve heard that they’re good too. Don’t waste time watching sketchy for bacteria, as that’s curriculum for Micro 2 and not 1. I did not read any immunology, however after the exam did I wish that I did. I think people usually read micro-related immunology on lectures or in the BRS book.

Sketchy micro for virus is amazing. They talk about basically everything you must know and make it really easy to remember stuff. Please pay for it to support them if you can.

You should know which antibiotics work and don’t work against gram positives and gram negatives, like how penicillin G and nafcillin works only on gram positives. You should know those antibiotics works against gram-negative cocci and those that work against gram-negative bacilli. You should definitely know which antibiotics work against MRSA, clostridium difficile and pseudomonas. I like this chart for this.

You should know which antibiotics you can’t give to children and pregnant women, and which that are nephrotoxic. You should know the mechanism of action for each antibiotic. You should know which types you can give orally. I wouldn’t waste time learning the names of too many drugs, just the major types and their most used examples. Don’t bother learning the names of the first three generation cephalosporins for example, but you should learn the names of generation 4 and 5, since there’s only one in each generation.

They do use the latin name for diseases instead of the common names, like they used condyloma acuminatum instead of “genital warts”, and they used erythema infectiosum instead of “fifth disease”.

Our group teacher gave us many sample tests and I looked through them all before the exam. We only got a couple of questions that were exactly the same as the sample test, but it was still very good to go through because the questions are similar.

The exam

The exam started at 12 in the lecture rooms. You have one and a half hour to do the exam, which is more than enough. Many were done before one hour had passed. There are 60 questions divided into four blocks. You need at least 9 correct answers out of 15 in each block to pass. I don’t know exactly what the four blocks are (they never tell you what they actually are!), but I think they are:

1. Bacteria (basic theory)
2. Virus
3. Antibiotics and disinfection
4. Immunology

There is some mix of vaccines and seminar questions (like agar stuff and staining and shit) in the different blocks. All 60 questions are single choice questions with just 4 alternatives.

They definitely did ask some questions I had no idea about (you can never be prepared for all possible questions), but overall was it fairly straightforward.

We got our grade on neptun before 14:00(!). I got a 4 after 6-7 days of effective reading.

I did make some flashcards for Micro 1. I don’t really think they’re greek.doctor-standard© but I’ll link to them here, here and here

Some questions I (kind of) remember

“A kid, 8 years old, has MRSA. He’s allergic to penicillin. Which antibiotic can you give?”

“A student has gram-negative cocci infection. Which antibiotic should you NOT give?”

“Which immunoglobulin is most abundant in the blood?”

“Which cells can present antigens?”

“Which cells can recognize antigens through MHC?”

“Which cells can recognize soluble antigens directly?”

“What causes erythema infectiosum?”

“Which of the following do not have nucleic acid? A: bacteria B: virus C: viroid D: prion”

The exam was last Friday, the 21st of December. My examiner was Dr. András Garami, and there was also a PhD student present as a co-examiner. The co-examiner just observed except for once, when the main examiner told the co-examiner to ask the student one question.

My topics were:

• Hypertension and the adrenal gland
• Pathophysiology of glomerular filtration
• Active heterotopic abnormalities (premature beats)

And the ECG of course. When you enter the room will you draw a green card, and on that card are your three topics. They didn’t give me the ECG until after I’ve been preparing my topics for at least 10 minutes. The examiner preferred to begin with the ECG so that’s what I did.

ECG

My seminar teacher told us to use that step-by-step approach on the ECG, and the examiner really liked it. I encourage you to do the same.

I determined that there was an RBBB and a type II AV block with Mobitz type II. However when I presented it to him did he show me that at some places was the PQ interval very small, meaning that it couldn’t have been a type II AV block. When he pointed that out did I immediately correct it by saying that it’s more probably a type III AV block with a ventricular escape rhythm. He told me that it’s not a ventricular escape rhythm. I realized my mistake again and said “No, this is not a ventricular rhythm because the QRS complexes are normal. It must therefore be a junctional escape rhythm.” He agreed, and asked me what could be done to fix this. After some back-and-forth did I arrive at the conclusion that a pacemaker was the right answer. We moved on to the theoretical topics.

Hypertension and the adrenal gland

I began with this because it’s my strongest theoretical topic of the ones I drew. I basically just explained to him what I’d already written. He then asked some questions. It went something like this:

• Garami: How is the blood pressure in Cushings in comparison to Conn syndrome?
• Nikolas: It should be lower, because cortisol has a weaker effect on mineralocorticoid receptors than aldosterone.
• G: That’s what you would think, but in real life it’s actually higher than in Conn syndrome.
• N: Really? I’m not sure.. [I spent some time thinking] Oh, is it because cortisol increases the sensitivity to catecholamines?
• G: Exactly. Now, how can we diagnose a pheochromocytoma?
• N: We can measure catecholamines breakdown products in the urine.
• G: Yes, how would you do that?
• N: Like, with a urine sample?
• G: Yes, but what else?
• [I didn’t really understand what he meant, but I think he wanted me to say that we should measure urine in a 24 hour period. I don’t really remember.]
• G: Okay, how does aldosterone increase the blood pressure?
• N: Well, you have increased salt and water retention that will cause the plasma volume to increase.
• G: Yes, but what happens to this volume?
• N: It stays in the plasma? I guess it could go into the interstitium if there was low oncotic pressure or the capillary hydrostatic pressure was increased for some reason.
• G: No, that’s not what I mean. There is no oedema. Will the vessels just continue to fill up with fluid? Wouldn’t they burst?
• N: Maybe the aldosterone receptors are desensitized after a while?
• G: No, that’s not what happens. Something “counteracts” the aldosterone.
• N: Oh, like the natriuretic peptides? Atrial natriuretic peptide and brain natriuruetic peptide?
• G: Yes. Why are they produced?
• N: Because of increased stretch of the atria and pressure receptors in the CNS?
• G: Yes. In fact, due to the increased plasma volume will organs vasoconstrict so that they aren’t overperfused. This means that the excess fluid doesn’t really reach the organs, but instead stays in the arterial system. Do you know what the mechanism where aldosterone is counteracted by natriuretic peptides is called?
• N: Aldosterone escape mechanism? [This was a half-guess. I’ve heard about aldosterone escape before, but I didn’t know that it’s this.]
• G: Yes! Great.

Pathophysiology of glomerular filtration

I don’t really remember what we talked about here. I explained what I’d written down, and he pointed out that I forgot to write that GFR also depends on the filtration pressure. He asked me to name an example for how TGF can cause problems for filtration (I think I said osmotic diuresis).

He disagreed that kidney stone, BPH or prostate adenoma would cause postrenal problems with filtration, as they would actually cause postrenal acute renal failure instead. He mentioned some better examples but I can’t remember which.

Active heterotopic abnormalities (premature beats)

Now, you might already notice that what I wrote was about a completely different topic. I’m really bad at the ECG topics (you might know that since I didn’t write about them), so when I drew that topic I became slightly panicked. I’ve looked through them the day before (Idun notes), and my girlfriend told me what active heterotopic means. However, I couldn’t come up with any examples, so I just wrote about fibrillation and flutter, because I thought that maybe they were a part of the topic (they technically are, but they have their own topic).

He instantly saw what I’d written and was very confused. He said “what’s this?” and that’s when I realized I’d fucked up completely. I tried to save it.

• N: Oh, maybe I should’ve written about extrasystoles and escape rhythms as well?
• G: Extrasystoles and tachycardias yes, but escape rhythms no. It even says “premature beats” in the topic name.

He asked me about types and classification of tachycardias (supraventricular and ventricular) and their compensatory pauses. He also asked me what Torsade de Points is, which is when I drew the spindle-like ECG you can see on my notes.

• G: If you can explain to me why the compensatory pause is different in ventricular and supraventricular tachycardias will I give you a 5.

I couldn’t. I didn’t even know they had different compensatory pauses. He tried really hard to make me “recall” why it was, but I’ve never learnt it so I couldn’t recall it. He eventually understood that I didn’t know the answer and gave up.

• G: I’ll give you the 5 anyway, as encouragement.

All in all was the experience very good, mostly the same as for patho. He was extremely nice and passed everyone, even those who failed to answer certain basic questions either because they didn’t know or they couldn’t recall the answer. Just be aware that they’ll always find ways to ask questions you are not prepared for. My notes (and the book and lectures) don’t cover absolutely everything, so you can’t be prepared for every possible question, but it’s still possible to get a 5.

So I had my pathology 1 exam today. It’s the first day of the exam period and my examiner was Dr. László Kereskai.

The exam begins with you drawing a theoretical topic inside an envelope from a box full of envelopes. They’ll then give you a prep, and they give you a number for the slides. On the computer are the slides numbered (from 100-150 or something), and they give you one number. I’m pretty sure they decide what your prep and slide should be based on your topic. When it was my turn was I told to begin with the slide, then the prep and lastly the topic.

My topics were:

• Clinicopathological classification of acute inflammation with organ examples
• Prostatic hyperplasia slide
• Rectal carcinoma prep

BPH slide

I began by saying that it’s HE stained, and that the urethral lumen and corpora amylacea show that this is the prostate. I then show the papillary structures and show the abnormal fibromuscular stroma (that I personally can’t see what’s normal about), and say that these are features of benign prostate hyperplasia.

I’ll try to include most of the conversation in bullet points. I’m N and he’s K

• K: Why is it called benign?
• N: To illustrate that it’s not a cancerous lesion.
• K: Yes. What types of syndromes can follow?
• N: Problems with urinating. Also, the bladder will be trabeculated because of hypertrophy.
• K: Yes. Do you think this patient was old or young? What was the age?
• N: Definitely old, perhaps 60-70.
• K: Perhaps even older. In the middle of a slide, there is a lobe. Do you know the name?
• N: I don’t.
• K: Okay, it’s called [Home lobe or something, I don’t remember]. Which zone of the prostate in hyperplastic?
• N: The central zone.
• K: Yes. How can you treat this if it causes symptoms?
• N: You can perform radical prostatectomy, wher-
• K: No no, we don’t do that for BPH, only for cancer. There’s something else.
• N: Oh, you can go into the urethra and scrape out the prostate.
• K: Yes, that’s right.

Rectal carcinoma prep

I begin by showing that there is a deep, ulcerating lesion, and the borders. He disagrees with the borders and say that only the top of the preparation shows unaffected mucosa.

• K: How would you describe the cancerous growth?
• N: It’s invasive and ulcerating?
• K: Yes, but what else
• N: It looks like many small polyps [This is more easily visible on the back of the preparation]
• K: Yes. What are the predisposing factors for this cancer?
• N: Inflammatory Bowel disease, like Crohn’s disease and Ulcerative colitis
• K: Yes, but they’re not the biggest.

I shouldn’t have begun by mentioning IBD, as they’re a very rare cause. I was just really eager to say Crohn’s disease.

• N: The biggest factor is the presence of polyps with dysplasia, adenomatous polyps. Not hyperplastic ones.
• K: Yes. How can you diagnose this?
• N: By endoscopy. Colonoscopy.
• K: Yes. We can use chemical methods as well but they’re not as good. It’s very uncomfortable so many people skimp on screening because of this, but it’s much better than cancer.
• N: I know it’s uncomfortable, I’ve performed it myself. It’s very uncomfortable.
• K: Yes, especially the day before.

We laugh

• K: What could the symptoms be?
• N: This is in the distal part of the colon, so we could see haematochezia, constipation and diarrhoea. If the cancer was in the ascending colon would the symptoms be different, mostly because the lumen there is wider.
• K: Yes, what about the lumen in this cancer?
• N: It will be smaller
• K: Yes, perhaps even completely blocked. Some endoscopies can’t get past the tumor because of this. Do you know the age of people that get this cancer?
• N: 20-30?

I still had Crohn’s disease in my mind, so I thought about the the age when people with Crohn’s usually get cancer.

• K: No not at all. Perhaps they’re born in 1920 and 1930. They’re very old

Great joke actually

• K: Do you know when we start to screen for colorectal cancer in Hungary?
• N: Around 50?

Pure guess

• K: Yes, around 55. What can the treatment be?
• N: Removal of the affected part or whole colon.
• K: Yes, if there’s no spreading.

Acute inflammation

• K: Tell me about the types
• N: You have serous inflammation, where the exudate is almost like transudate, with low protein content.
• K: Can you name an organ example?
• N: Acute rhinitis?

I was very unsure about that answer

• K: Yes. There is a particular disease group that commonly affects serous membranes. Do you know which?
• N: No, I can’t recall.
• K: Autoimmune diseases. Now, what about fibrinous inflammation?
• N: It’s often due to more severe infections. The capillary permeability is increased enough that fibrin can enter the interstitial space.
• K: Can you name an example?
• N: Fibrinous pericardits
• K: What’s the most important cause of that?
• N: Acute myocardial infarction
• K: Yes, definitely. Can you mention another cause?
• N: Bacterial infection?
• K: No, no. There’s something else.
• N: I don’t recall anything.
• K: There was a story written on the fibrinous pericarditis preparation. It was taken from a woman with kidney failure, which ca-
• N: Oh, uraemia!
• K: Yes, uraemia is the other big cause of fibrinous pericarditis. Indeed is infection not a normal cause for that.
• K: What about haemorrhagic inflammation?
• N: Here will the exudate contain blood as well.
• K: Can you name any examples?

I was hoping he wouldn’t ask that

• N: Pneumonias?
• K: Yes, what types?
• N: Bacterial?
• K: No, no. Rather viral. There is a special organ that is characteristic for haemorrhagic inflammation. Which?
• N: I don’t know.
• K: The bladder, actually. Okay, what about pseudomembranous inflammation?
• N: It’s due to diphteriae or clostridium difficile, and commonly occurs in colon and upper airways.
• K: Yes, diphteriae in the upper aiways and clostridium in the colon. What is the cause of pseudomembranous colitis?
• N: Antibiotic treatment
• K: Yes. What do you think is the treatment for it?
• N: Other antibiotics that are specific for clostridium?

Qualified guessing by me

• K: Yes. It’s caused by antibiotics but we treat it with antibiotics. We use [some types I don’t remember]. What about purulent inflammation?
• N: We have three types, empyema, phlegmone and abscess.
• K: Can you name an example for empyema?
• N: Yes, like purulent meningitis.
• K: Yes, and for phlegmone?
• N: It can occur in soft tissue, or walls of organs like in acute appendicitis.
• K: What can acute appendicitis lead to?
• N: A periappendicular abscess.
• K: Yes, but that’s not the most common. Something else can happen
• N: I can’t remember
• K: It can become gangrenous inflammation.

That’s the end of what I remember. I obviously used a lot of time to think when he asked questions, and sometimes he had to help me find the answer. The whole thing took about 15 minutes I’d say.

I was really lucky with my topics. Also, I sat next to the cabinet with the preparations, so when I needed some organ examples for acute inflammations I just turned around and checked some preps 😂

Dr. Kereskai asked all of us many clinical questions, like what are the symptoms, what are the risk factors, how can you diagnose it, how can you treat it etc. I was told that he really likes immunology but he didn’t talk to me about that at all. He didn’t ask about definitions, not for hyperplasia or inflammation, or the signs of inflammation or anything like that.

All in all, he was really nice, and so was the other examiner in the room (for the most part). Everyone in the room passed, despite some not knowing certain things and answering wrong to some questions. We all did.

I got 4, 4 and 4/5 on my topics (don’t remember which one was 4/5, I believe it was the prep). The end grade was 4.

I’d encourage everyone to never begin with the diagnosis on the slide and prep. Instead, start with the staining, show some healthy tissue (if present), say the organ, show the abnormalities, and then come with the diagnosis. Also, they were really nice. I’m certain that anyone who has studied pathology 1 well can pass it without too much problem.

My next exam is pathophysiology 1 next Wednesday (unless I can get a spot on next Friday. Hit be up if you don’t want your spot next Friday).

Edit: Here are the exam notes of my girlfriend, who got a 5