The nasty flu bug has hit our household, and I need to stay home tomorrow with a sick child. So - we will not be having our exam review tomorrow from 11:15 - 12:05. Instead, I have beefed up the presentation I was going to give, and put in lots of study questions, with answers in the notes section (beneath the slide), and explanatory slides following each question. Being that we just had a quiz on Renal and GI a few days ago, I focused on Heart and Lung in the review. You can find the updated reveiw on our Reviews page. Let me know if you have any questions on the material; I'll answer individually and also post questions (anonymously) and answers here.
Question on Dr. Pacala's material
11.02.09
Q. Dr. Pacala's lecture has a lot of information on different medications. What would you like for us to take from the information?
A. Don't memorize the names of drugs at all - or the doses, or conditions you'd use them for! Dr. Pacala mentioned these so you will have heard of them; he meant it as a background-knowledge type of information. I would like it if you understood the philosophy that he discussed regarding treatment of medical conditions in elderly, frail patients. I think it's summarized well on slides 35 (in which he shows how you might treat an elderly, frail patient: you'd consider what the treatment goals were, and possibly relax your normal standards a bit, treating a little less aggressively) and 38 (last line: tailor treatment to condition of the patient - in other words: consider the side effects of the various treatments, and if the patient is frail, make sure the side effects of the treatment aren't worse than the disease itself).
More questions and answers
11.02.09
Q. Is a fibrofatty atheroma the same as a fibrous cap?
A. “Fibrofatty atheroma” describes the whole lesion (lipid/necrotic core with overlying fibrous layer); “fibrous cap” describes just the top fibrous layer. Slide 18 of the Cardiac Pathology 1 powerpoint has a drawing of a fibrofatty atheroma. It kind of looks like the line is pointing at the fibrous cap – but it is meant to denote the entire lesion.
Q. Since Wegener Granulomatosis has the typical triad but not all aspects do not need to be affected, would the only way to definitively tell the difference between Wegener's (if not presenting renal dysfunction) and Churg-Strauss is testing for either the p or c-ANCA?
A. The ANCA tests would be highly suggestive of either Wegener’s or Churg-Strauss (most patients with Wegener’s have p-ANCA, and most patients with Churg-Strauss have c-ANCA) – but there are (of course) exceptions to that rule. So you’d have to combine the ANCA testing with the clinical symptoms. Like you mentioned, there is considerable overlap between the two – and the symptoms are not always classic. In Churg-Strauss, there is an association with allergy and asthma, which may help differentiate the two. So the bottom line is: the two are similar, and often have overlapping symptoms, and there is no one definitive test – but the ANCA testing is usually very helpful.
Q. Can VSD and PDA also lead to the same pulmonary problems as ASD since they are all left to right shunts?
A. Yes! Any left-to-right shunt, if it is big enough, can eventually put enough pressure on the right side of the circulation that the lungs respond by constricting vessels and laying down fibrotic tissue, leading to pulmonary hypertension. Eventually, if pressures on the right side exceed those on the left, the shunt reverses, becoming a right-to-left shunt.
Q. What is the effect/outcome of the overriding aorta in Tetralogy of Fallot?
A. The main problem in Tetralogy of Fallot is the pulmonary outflow obstruction – that really determines the extent and severity of the clinical picture. The overriding aorta doesn’t contribute much. It does allow unoxygenated blood to flow directly into the aorta, which doesn’t help matters. There already is a ventricular septal defect, which allows mixing of blood, so the overriding aorta would just exacerbate that mixing, making it even easier for blood to bypass the lungs and go straight to the peripheral circulation. Which manifests as cyanosis.
Q. Can you surgically repair TGA?
Yes. Patients with TGA usually have some sort of shunt as well (like a VSD) – and depending on the degree of shunting, they may be fairly stable for a little while. However, most of the time, the transposition is repaired surgically within weeks of birth.
Q. How well should we know the morphological changes (table) in a MI?
A. Slide 36 of the Cardiac Pathology II lecture has a table with a bunch of morphologic changes – I’m assuming you’re referring to that table. I would like you to know the microscopic changes, not the macroscopic ones. The macroscopic changes are not that definitive – I just think it’s interesting to see how what’s going on microscopically is reflected in the gross appearance of the heart.
Q. Is mitral valve prolapse an insufficiency since it cannot close properly?
A. Yes – that’s exactly right. Insufficiency means the valve can’t close properly; stenosis means it can’t open properly. In mitral valve prolapse, the leaflets are floppy, and they don’t come together like they should, so during diastole, blood regurgitates into the left atrium.
Q. How is atypical chest pain of pericarditis different than, say, angina?
A. This is a great question – and one that is not easy to answer, because the term is not well defined, and nobody seems to agree on how to make it less confusing. One way to define “atypical chest pain” is to say that it is any type of chest pain that is not “typical” of ischemia (crushing, strangling chest pain with occasional radiation to the left arm, often accompanied by nausea, vomiting, or sweating). “Atypical” chest pain would then include chest pain that’s made worse by inspiration, by lying down or standing up, or pain that is reproducible with palpation. It implies that the cause of the pain is not due to an acute myocardial infarction. It’s a very gray area, and one that requires a lot of clinical experience.
Q. I know that azotemia is associated with increased BUN and increased creatinine, but is it also associated with increased GFR?
A. No - azotemia is associated with a decreased glomerular filtration rate. Whatever is causing the azotemia is causing less blood to flow through the glomerulus (or another way to think of it is that the pressure of blood within the glomerular vessels is lower), which means that the things that should be filtered out of the blood and into the urine (like BUN and creatinine) are staying in the blood.
Q. With minimal change disease, podocytes coalesce. Would that lead to a decrease in urine secretion?
A. You’re right: in minimal change disease (and in other conditions causing the nephrotic syndrome) podocytes (or foot processes) coalesce. But no – that does not lead to a decrease in urine secretion! You’d think it would! Plus, these patients actually pee out MORE protein – which doesn’t make sense either.
Even more questions and answers
11.02.09
Q. If patient has membranous glomerulonephritis, will all glomeruli be effected or just some? Both kidneys or just one kidney? Also, what are the deposits made of?
A. In membranous glomerulonephritis (and in most of the other glomerular diseases too, except for focal segmental glomerulosclerosis), most or all of the glomeruli will be affected, and both kidneys will be involved. The deposits contain immunoglobulin and complement.
Q. What is the difference between oliguria and dysuria?
A. Oliguria means decreased urine output; dysuria means it hurts when you urinate.
Q. Does benign nephrosclerosis cause irreversible damage?
A. Yes, it can. Most of the time, it doesn’t cause enough damage to cause renal failure. But there are morphologic changes that are irreversible: hyalinization of blood vessels and scarring of the kidney.
Q. Is hematuria usually painful?
A. It can be either painless or painful. Common causes of painful hematuria are kidney stones and kidney infection; painless hematuria may be associated with renal carcinoma.
Q. Should we know the four presentation of bladder carcinoma?
A. No – just know that the deeper the carcinoma is, the worse the prognosis is. Which makes sense.
Q. If achalasia describes dilation, how can the sphincter be closed? Or is it that the esophogaus is dilated/ enlarged and the sphincter is closed (kind of like a balloon)?
A. Achalasia means that the esophageal sphincter is unable to relax – so it’s always sort of tightened. The esophagus is dilated, just like you mentioned – like a balloon.
Q. Is villous adenoma more dangerous/carcinogenic than tubulovillous adenoma?
A. Theoretically, yes. Villous adenomas are more likely to turn into carcinoma than are tubular adenomas - so tubulovillous adenomas would be somewhere in between. However – the contribution of the architecture (villous vs. tubular) is less important than the size of the adenoma – the bigger the adenoma, the more likely it is to develop into carcinoma.
Q. From the lung clinical correlations lecture, should I focus on the stepwise therapy for asthma and what from the lung infections table should I focus on?
A. I would not focus on either of these for the test – the questions from the clinical correlation lectures will be much more general and will not include specific therapeutic details (like which meds you would use to treat different conditions).
E. coli beef recall
11.02.09
Here's an example of what we talked about in class with E. coli O157:H7 causing hemorrhagic colitis and hemolytic uremic syndrome. Half a million pounds of beef have been recalled because of possible contamination with E. coli. The outbreak is associated with 2 deaths so far, and it's mostly in the Northeastern US. Ugh! Be very careful with ground beef - if you have to use it, cook it until there is absolutely no pink in it!
iPhone health professional apps
11.02.09
If you have an iPhone, you probably check the app store about every 10 minutes. Well, maybe not that often. But it's so much fun! The health category is ever-expanding, and most of it seems to be repeats of the same old thing - drug dose calculators, calorie trackers, pocket first aid, and period trackers. It's hard to find good apps among all the hundreds of banal ones. Here's an abbreviated list of some good medical apps. There are a few dental ones, including one 3D one that looks pretty cool. How about you - what is on your iPhone, if you have one? Here's what's on mine.
Next week we'll be talking about the different kinds of leukemia, one of which is chronic myeloid leukemia (CML). This used to be a fatal disease, but a recently-created drug, Gleevec (generic name: imatinib), has changed it into a manageable chronic disease. Here is a New York Times interview with the inventor of this truly miraculous drug, Dr. Brian J. Druker. I like this quote from Dr. Druker: "The way I’d been trained, cancer was seen as something like a light switch that was stuck in an 'on' position. You were given a baseball bat, which was chemotherapy, and told to knock the light out with the bat. I thought, 'Why don’t we just try to figure out why the light is stuck on, then we can fix it without breaking everything.'" Thanks so much to the student who sent this along!
Exam 2 results
11.05.09
The results for exam 2 are now posted. I dropped two questions (making the total for this test 53 points) because not very many people got them correct, and I think they may have been too obscure. The two questions are:
ARDS (acute respiratory distress syndrome) or diffuse alveolar damage can be caused by all of the conditions listed below EXCEPT:
A.Gastric fluid aspiration
B.Pulmonary emboli
C.Mechanical trauma (including head injuries)
D.Sepsis
E.Diffuse pulmonary infection by viruses
Answer: B
12. Golden-brown, beaded, dumbbell-shaped, elongated bodies measuring 10-50 micrometers in length, strongly staining with iron were found in the lung parenchyma of a patient with lung cancer. He was a smoker. However, this histologic finding indicates that he was also exposed to another cancer-inducing substance. Which of the following is most likely to be that cancer-inducing substance?
A.Asbestos
B.Beryllium
C.Coal
D.Iron
E.Silica
Answer: A
If you got one or both these questions correct, I will add the correct number of points to a points bank, and if at the end of the course you are very close to the next-highest grade, we'll add these points to your overall score.
Boards review questions
11.05.09
Starting a new series of posts here. Periodically I will post some questions that are similar to those I've seen as I reviewed board review materials. I use First Aid, Dental Decks, and Dental Stax, and I can't reprint their questions, obviously, but I've created ones that are similar enough so you can get an idea of what you should be thinking about when boards time comes.
Our first installment is on GI and liver pathology. These should be easy! There are a few that we didn't cover - but we ran out of time as it was. How do they expect us to cover all of this stuff? Seriously. After you look at the questions, check out the answer page.
1. Common hepatitis infections include Hepatitis A, B, and C. Which of these is the least serious?
A. Hepatitis A
B. Hepatitis B
C. Hepatitis C
2. All of the following are true regarding cirrhosis except:
A. It is a chronic disease characterized by destruction and regeneration of liver cells
B. The male:female ratio is 1:2
C. It is especially common in malnourished people over age 50 with chronic alcoholism
D. Many patients die within 5 years of diagnosis
3. Jaundice is a yellow discoloration of the skin, mucous membranes and eyes. It is caused by an excess of what in the blood?
A. Glucose
B. Creatinine
C. Bilirubin
D. Folate
4. Which of the following predisposes to esophageal varices?
A. Mallory-Weiss syndrome
B. Hemolytic anemia
C. Portal hypertension
D. Barrett esophagus
5. In which part of the GI tract are malignancies most common?
Gastric fluid aspiration
