My Pathophysiology 1 exam experience

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.


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.

My Pathology 1 exam experience

Last updated on December 12, 2018 at 19:21

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
My notes for the prep (left) and slide (right).

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

Notes for theoretical question. Yes, I forgot about gangrenous inflammation and remembered no examples for haemorrhagic.
  • 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