Quiz 3 is a take-at-home, online quiz. It’s on Google Forms, and the link is here. It will be open from now until midnight on Friday (11/18). Let me know if you have any questions or any problems!
In case you’re interested, I have a few books on blood disorders and coag that students have found helpful in the past:
- One on hematopathology (anemias, leukemias, other diseases)
- One on coagulation (clotting, bleeding disorders, thrombotic disorders)
- One that includes most of the hematology posts on Pathology Student
- A little one that just covers the most important anemias for you to know.
These are all for sale but I don’t want you guys to have to buy them. If you would like a copy, drop me an email and I’ll send you a link so you can download them for free. They are NOT required – so just use them to help you study (if you feel you need help).
You guys did really well on Exam 2! The mean was 96%! Nice job 🙂 There weren’t any problematic questions, so nothing needed adjusting. Scores are now posted on Canvas.
We’ll talk about amyotrophic lateral sclerosis (ALS), sometimes called Lou Gehrig’s disease, tomorrow. It’s a pretty fast-progressing disease of motor neurons, with most patients dying within 5 years.
Stephen Hawking was diagnosed with ALS when he was 21, and he lived until the age of 76 (he died in 2018). What?? Here’s an article from Scientific American that talks a bit about some of the reasons he may have beaten the odds like this.
Also – there is new research showing that inherited cases of ALS are caused by buildup of a toxic protein called SPOP within neurons. AND there are drugs that can inhibit or get rid of this protein (in mice, but hopefully soon in humans too). This research is so exciting, because it may lead to greater understanding of what goes on in the sporadic cases of ALS, which are much more common than the inherited versions. There is hope!
This is one of those blow-your-mind TED talks. Jill Bolte Taylor, a brain researcher, had a stroke. But it wasn’t an ordinary stroke. Because of her training, and her insight into the way the brain works, she actually watched – calmly and with curiosity – as her brain functions shut down, one by one. Not only that, but she felt she attained a new level of consciousness beyond left brain/right brain – and said it was lovely. Totally fascinating.
How about you – have you seen any TED talks that you found fascinating? If so, I’d love to know. It’s great if they’re about medical stuff – but I’m interested to hear about non-medical ones too.
I’ll mention this very informative – and sad – New York Times story in class tomorrow. It involves a young woman named Katharine Moser who decided to undergo genetic testing to see if she carried the gene for Huntington disease.
Katharine recalls how her family considered the disease to be a curse – a shameful thing not to be mentioned. Strangers showed a remarkable lack of compassion, assuming that her grandfather’s unsteady gait (an early symptom of the disease) meant he was drunk. Her mother was appalled at Katharine’s interest in being tested for the disease; if Katharine carried the gene, that meant her mother did too – and her mother did not want to know.
Here is a video talking about how people who have a family history of Huntington disease are more open about the disease now than their parents or grandparents were. There seems to be a lessening of the shame and stigma that has typically been associated with Huntington disease. Good! How ridiculous it is to view a genetic disease as shameful.
There are several short scenes in this video showing patients with Huntington disease, and if you watch carefully, you will notice some of the involuntary movements typical of Huntington disease. These short, unpredictable movements may be jerky or more writhing in nature. They are called “choreiform” movements (from the Greek “chorea” or dance).
You guys did great on Exam 1, as usual! The mean was 93%. There weren’t any problematic questions – so no points were adjusted. You should see your score in Canvas now, and you should also see your exam report (which tells you which questions you got wrong, if any!) in your Examsoft Student Portal. If you have any questions about the exam, or just want to take a look at it, let me know and we can find a time to do that.
I also went back to quiz 1 and adjusted those scores to reflect this question, which was keyed incorrectly:
Which of the following bacteria is the most common cause of community-acquired pneumonia?
A. Staphylococcus aureus
B. Haemophilus influenzae
C. Streptococcus pneumoniae
D. Mycoplasma pneumonia
The correct answer is Streptococcus pneumoniae. However, when we did the quiz in class, Staphylococcus aureus was accidentally marked as the correct answer.
My first “fix” was to add a point to everyone’s score, which is what I usually do when a question is really hard. But this didn’t fix the problem, as one of you very kindly pointed out to me. It didn’t give credit to the students who answered the question correctly!
So today I fixed the scores correctly…if you’re still reading I’m impressed…I rescored the quiz using the correct answer for that question, and I also added an extra point to everyone’s score because the whole thing was just so irritating.
That’s about it for now! Check Canvas when you have a moment and let me know if something doesn’t look right to you.
Here is some information about Exam 1.
The exam will be delivered by ExamSoft like we have done in our previous courses. It will be available all day on Wednesday, 10/12/21 (from 12:01 am until 11:59 pm). You’ll have 2 hours to take it once you open it, and you’ll need to submit it by 11:59 pm.
If you have exam accommodations, could you please send me a quick email reminder? I just want to be sure I get everyone’s timings correct. Thank you!
Here’s the breakdown by content (I broke the heart lectures down further into subtopics):
- Blood vessel pathology – 5 questions
- Heart failure – 1 question
- Congenital heart diseases – 2 questions
- Ischemic heart disease – 3 questions
- Heart valve disease – 1 question
- Cardiomyopathy – 1 question
- Respiratory pathology – 5 questions
- Renal pathology – 7 questions
- Upper GI pathology – 2 questions
- Lower GI pathology – 3 questions
- Pancreas, Liver, and Gallbladder pathology (slides 1-37) – 3 questions
- Pancreas, Liver, and Gallbladder pathology (slides 38-51) – 2 questions (see below!)
Specific testing topics from part 2 of the Pancreas, Liver and Gallbladder lecture
Since slides 38-51 of the Pancreas, Liver and Gallbladder lecture were only covered today, and it’s very close to exam time, I’d like to let you know which of these slides to focus on for the exam. In class, I mentioned 3 topics, but I decided to make it even more focused. There will be one exam question on each of these 2 topics:
1. Acute Pancreatitis
Here is the slide that covers this topic:
2. Pancreatic Carcinoma
Here is the slide that covers this topic:
I’ll post the password shortly before the exam starts on Wednesday. Please let me know if you have any questions!
One of the things we talked about last week in our Renal Path lecture was nephritic and nephrotic syndromes. I thought it might help to review them a bit, since they can be maddeningly frustrating if you don’t understand the underlying principle in each one.
So here are the four main characteristics of each:
- Massive proteinuria
How do you make these lists hang together in a way that you can remember?
First, let’s take nephrotic syndrome. The thing to remember for this one is massive proteinuria. You might do this by remembering that nephrotic and protein both have an “o” in them. The massive proteinuria in these patients leads to hypoalbuminemia (they are peeing out albumin!), which results in edema (the oncotic pressure in the blood goes down, and fluid leaks out of the vasculature into the surrounding tissue). So right there, you have three of the four features, just by remembering one. The hyperlipidemia/hyperlipiduria occurs because as the liver is trying to make more albumin (to make up for the albumin loss in the urine), it also ends up making more lipids. As an aside, nephrotic syndrome is often more dangerous than nephritic syndrome, so you might want to think of this syndrome as the “oh sh*t” syndrome (again – nephrotic has an o in it, nephritic does not). Crude, but if it works, who cares?
In nephritic syndrome, there is some proteinuria and edema, but it’s not nearly as severe as in nephrotic syndrome. The thing with nephritic syndrome is that the lesions causing it all have increased cellularity within the glomeruli, accompanied by a leukocytic infiltrate (hence the suffix “-itic”). The inflammation injures capillary walls, permitting escape of red cells into urine. Hemodynamic changes cause a decreased glomerular filtration rate (manifested clinically as oliguria and azotemia). The hypertension seen in nephritic syndrome is probably a result of fluid retention and increased renin released from ischemic kidneys.
If you really want to pare it down – if you only have enough brain space to remember one feature for each disorder – remember that nephrotic syndrome is characterized by massive proteinuria (the “o” in nephrotic), and nephritic syndrome is characterized by inflammation (the “-itic” in nephritic). Then at least you’ll have a shot at remembering the other features.
On Monday 10/10, we’ll be doing an in-class exam review (using Kahoot, as usual). Before we do that, I’ll spend about 15 minutes finishing up the last 13 slides from the Pancreas, Liver and Gallbladder lecture. There are only 4 diseases in those slides, so it will be quick. I’ve updated our lecture page to reflect this change.