Q&A
Your questions/Our answers
Spring 2008
Q&A's are emailed to you throughout the semester, but instead of having to dig through your emailbox weeks later to verify some detail, you can check this page!!
DR. SELF:
During the post-strep ST case, a student mentioned that it was taught in another course that strep skin infections were more likely to result in post-strep kidney disease, while pharyngeal strep was more likely to result in valvular disease. Is this correct?
Dr. Self replied:
No. Post strep GN can follow strep pharyngitis or impetigo. In
colder climates and during winter and spring, pharyngitis is more often the
cause. In summer and early fall and in warm climates, impetigo is more
often the cause. Maybe the mix-up is because rheumatic fever is usually
associated with strep pharyngitis and not impetigo. Post strep gn is
associated with both.
DR. LEWIN:
First, there is a “typo” on page 92. The answers to questions 2 & 3 should be A-E (not B-F). If you correct that, the answers will make a LOT more sense. Now for the Q&A:
A student asked: Pg. 99 has Centrilobular as (Zone 1) and Periportal as (Zone 3). The book seems to suggest to me on pg. 632 that the centrilobular zone surrounds the central vein and is Zone 3 while the Periportal zone is Zone 1. Can you set me straight?
Dr. Lewin replied: The book is correct, centrilobular is zone 3.
A student asked: I've got a question relating to Question 10 in the Intrahepatic
Biliary /Circulatory lecture on pg. 108 of the syllabus.
The symptoms seem a very clear description of PSC. The question
states "What underlying disease best explains these findings". It
would seem to me that PSC would be the answer, however UC is given as the
correct. Although there is a high correlation between those having
PSC and UC it seems to me that the hepatic findings are best explained by
PSC since UC doesn't cause any hepatic problems in and of itself.
Dr. Lewin replied: You are correct that PSC would be the best answer (unfortunately it is not one of the choices, PBC which is not correct is). We are left with UC (and the inference that the individual also has PSC with which it can be associated). The question is trying to get people to make that second leap (knowing the features of PSC and then also that UC is associated with it).
A student asked: I'm confused on the concept of the false negative that occurs with hypertriglyceridemia. Also, can explain what the "double duct" sign is again?
Dr. Lewin replied: Hypertriglyceridemia - triglyceride concentration greater than 1000 mg/L may interfere with the enzyme -substrate reaction causing a low reading (False negative). Increased in vivo triglycerides may induce pancreatitis but their presence in high concentration inhibits the amylase assay. From above, the laboratory assay for amylase takes advantage of the enzymatic activity of amylase to cleave a marker substrate. Increased triglycerides in the serum (which is what is put into the assay) interferes with this laboratory assay and may give a falsely negative amylase value (the substrate will not be cleaved, suggesting there is not amylase in the serum, when actually it is increased).
The double-duct sign is dilatation of both the pancreatic and common bile duct. It suggests there is something obstructing both ducts and is a marker for carcinoma of the head of the pancreas (either pancreatic or of the common bile duct), although a stone in the ampulla of Vater could give the same radiographic findings.
A student asked: I'm confused as to why # 8 at the end of the pancreas lecture isn't E, all of the above. On p. 681, it says that calcifications can be visualized. Also, on p. 681, it mentions that mononuclear inflammatory cells can be involved too.
Dr. Lewin replied: If I have the correct question:
__8. The pathogenesis of pancreatitis is?
A. Self digestion of the pancreatic
tissue
B. Overwhelming inflammation
C. Dystrophic calcification
D. All of the above
E. None of the above
The answer is all of the above (the question has this as answer "D", not "E"). The regular exam will not have questions put in this type of confusing difficult format.
A student asked: I had a question on 2 of the practice questions from the liver function tests section:
Dr. Lewin replied: A 53-year-old postmenopausal woman has been feeling tired
for several months. She has had some mid-epigastric pain for the past month.
Laboratory findings include: WBC count 6300/uL, Hgb 12.0 g/dL, Hct 35.5%, MCV
78 fL, platelets 236,000/uL, total protein 6.0 g/dL, albumin 3.5 g/dL, alkaline
phosphatase 270 U/L, AST 84 U/L, ALT 35 U/L, lipase 45 U/L, total bilirubin
1.1 mg/dL, and direct bilirubin 0.8 mg/dL. Her stool is positive for occult
blood. Which of the following conditions best explains these findings:
A Hepatic
metastases
B Wilson's
disease
C Acute
hepatitis A
D Acetaminophen
toxicity
E Congestive
heart failure
For this case it is more a function of exclusion and using the additional
information. The anemia and occult blood suggest colon cancer, that with liver
enzyme abnormalities suggest metastatic cancer.
Looking at the liver enzyme abnormalities, there is greater alk phos elevation
than AST/ALT, suggesting biliary, however the bilirubin is normal. Congestive
heart failure, acetaminophen toxicity and acute hepatitis A should all have
AST/ALT elevations that are higher and less alk phos elevation. Wilson's disease
can have a variable presentation, however should have additional findings of
decreased ceruloplasim and elevated liver copper.
Gilbert's syndrome individuals have decreased hepatic levels of glucuronosyltransferase. Stress (ie. Crash diet) appears to cause increased bilirubin either through increased production (ie. Red cell destruction) or added hepatocellular dysfunction.
A student asked: I just have a quick question about Hepatocellular Carcinoma. In the fibrolamellar variant the book says that AFP is elevated in 50% of cases but our notes say 60-75% of cases and the book says that it tends to occur in individuals 20-40years of age and I have 50-60years of age in my notes. Any help in clearing up the confusion would be greatly appreciated. Thanks for your time!
Dr. Lewin replied: I would go with the book. Fibrolamellar variant occurs in a younger age (I thought the mean age was 40, however the book has it as 20-40), in non-cirrhotic livers and has a better prognosis. The AFP elevation of 50% in the book is for all HCC (not just fibrolamellar variant). Fibrolamellar variant will have elevated AFP's, however they rarely get above 250 (regular HCC's can have AFP's in the thousands).
A student asked: In the syllabus on p.92 there are some very confusing elements.
For number 1, where did CHF come from? There was no mention of it in the entire lecture and how does it relate to the stem of the question? What am I missing? For number 3, I just wanted to make you aware that kernicterus is caused by UNCONJUGATED hyperbilirubinemia (neonates have decreased UDP glucuronyl transferase). Also, some teachers are no longer using the term stercobilinogen since it is identical to urobilinogen (a useless distinction that causes confusion).
Dr. Lewin replied: Regarding CHF: I believe the answer in this instance is hepatic metastasis (not CHF), so CHF was put in as a distracter. Admittedly I did not talk about hepatic metastasis in the lecture, with the exception of reviewing this question. For number 3: I just wanted to make you aware that kernicterus is caused by UNCONJUGATED hyperbilirubinemia (neonates have decreased UDP glucuronyl transferase). This is supposed to be the answer for this question (and is in my original material). Regarding the term stercobilinogen: Noted, the current Robins is using this terminology, although the handout still had an old chart. It will be removed in subsequent years (although I must admit the concept of urobilinogen in the colon seems like an oxymoron as itA student asked: I have a question regarding
number 12 on page 72 of the syllabus. You have the answer as b, which states a 5 year survival rate
of 90%
(following resection of an adenocarcinoma), but the book says it has a 5 year
survival of less than 20% (p. 598). Am I interpreting this wrong? Could
you
please clarify?
Dr. Lewin replied: It all depends on the stage. Overall the
5 year survival rate
is less than 20% (for all comers), however an early stage tumor(confined to
the
mucosa) with surgical resection has an excellent 5 year survival. Unfortunately
these tumors are relatively uncommon and most individuals present with much
higher stage lesions.
A student asked: On page 113 of the syllabus, question 4
states the most common type of cancer in the small intestine is an adenocarcinoma. However,
Robins
doesn't really make a distinction saying that "adenocarcinomas and carcinoids
have a roughly equal incidence" (p. 625). Also, the Goljan Rapid
Review book
says that carcinoids are the most common in the small intestine. Which
of
these is correct?
Dr. Lewin replied: You are correct, this is not a great question.
Robbin's changed it's discussion, the previous edition had adenocarcinoma as
the most
common malignancy (I had always taken it to be about 50% of the cancers of
the
small bowel). Carcinoids are most often seen in the appendix and small bowel.
A student asked: For question number 3, how can end stage pancreatitis cause hypoalbuminemia edema?
Dr. Lewin replied: This is a function of severe malabsorption associated with chronic pancreatitis. Protein malabsorption will lead to hypoalbuminemia (the major protein in the blood) and then edema.
A student asked: For question 8, why can't the answer be "D" all of the above? I thought with pancreatitis you get an inflammatory response and you can also get calcification in chronic pancreatitis.
Dr. Lewin replied: The pathogenesis is essentially self digestion of the pancreas. The inflammatory infiltrate is typically negligible (except in rare autoimmune pancreatitis) and calcification is thought to be a secondary rather than primary pathogenic mechanism.
A student asked: For question 10, can you explain what in the question stem would lead me to a diagnosis of pancreatic adenocarcinoma? I thought she would have primary biliary cirrhosis.
Dr. Lewin replied: The findings (given the marked elevation of bilirubin) are most consistent with an obstructive process (stone or pancreatic head mass). PBC typically does not have bilirubin elevations that high.
A student asked: I'm a bit confused by the mixed stones. The book does not seem to mention them. I understand from your lecture that they are the most common stones - is this true? Also what are they made of (is it just a mixture of cholesterol and pigment stones?)? Are they radio-opaque or lucent?
Dr. Lewin replied: Sorry about the confusion. This came from previous Robbins texts that divided stones into pure cholesterol, mixed (meaning cholesterol and bile salts), and pigment (containing bilirubin calcium salts). Mixed can be used synonymously with cholesterol stones in the text (radiolucent).
A student asked: Should we memorize the chromosomes for things like hemochromatosis and Wilson’s disease? (or any of the pediatric liver diseases).
Dr. Lewin replied: No need to memorize chromosome numbers for the genetic disorders for my part (I am not sure if they come up in another course, so don't shoot me if they are in the exam, they are not part of my questions).
A student asked: I was wondering about which is the most common type of gallstones. The book and internet seem to say that it is cholesterol, but question 3 on p. 111 says that the correct answer is mixed. Could you please clarify?
Dr. Lewin replied: Unfortunately Robbins changed this on me. Previous editions had subdivided into pure cholesterol, mixed (which contain cholesterol) and pigment. Mixed are the most common. This will not be on the exam.
Answers to Dr. Smith’s Handout Review Questions
1. A
2. D
3. D
4. D
5. C
6. A
7. A
8. C
9. B
10. D
11. A & C
12. A
13. D
14. B
1. C
2. D
3. G
4. F
5. B
6. A
7. E
8. H
9. I
A student asked: I have a quick question about p. 413 and p. 422 in the syllabus. If you answered this question already or if it's answered later in the syllabus, then just let me know that I haven't gotten there yet please! :) On p. 413, it says that functioning neoplasms result in atrophy of adjacent adrenal cortex 2ary to suppression of endogenous ACTH by increased cortisol levels. But on page 422, it says that adjacent cortex is of normal thickness due to no suppression of ACTH secretion by cortisol. What am I missing here? Thanks so much for clarifying this!
Dr. Caplan replied:
– the key here is whether the tumor is functioning – meaning that it produces cortisol. If an adrenal tumor is functioning – producing cortisol – then it will feed back negatively on the hypothalamus and pituitary so that the output of ACTH by the normal corticotrophs (ACTH-producing cells) in the pituitary will be reduced, resulting in less stimulation of the normal (nonneoplastic) adrenal cortical cells. This is what results in atrophy of the adjacent nonneoplastic and contralateral adrenal cortex. This is what I am describing on p. 413 – a functioning adrenal neoplasm (usually an adenoma) resulting in Cushing syndrome.
On the other hand, what I am talking about on p. 422 is a nonfunctioning adrenal cortical neoplasm – one that does not produce any hormones (and specifically, does not make cortisol). In this situation, there is no feedback inhibition exerted on the hypothalamus and pituitary gland; therefore, the output of ACTH remains normal and there is no reason for the adjacent or contralateral adrenal cortex to be atrophic. It is of normal thickness.
The other point I am making on p. 422 is that although functioning adrenal cortical neoplasms are capable of causing Cushing syndrome, primary hyperaldosteronism, or virilizing syndromes, it turns out that the majority of adrenal cortical tumors in fact are nonfunctional; most of these are discovered entirely by accident on an imaging study, such as a CT scan, for an entirely unrelated problem (for example, monitoring the size of a known abdominal aortic aneurysm).