SUMMARY
Question 31 will be given all credit; Question 76 - a or b will be accepted.
In addition, we will give a two point adjustment for test difficulty. This is partly motivated by some excellent challenges showing how knowledge of information from outside sources might invalidate certain questions, and partly in acknowledgement that the exam was a little more difficult than last year. This allotment won't be reflected in the exam score, but rather by a reduction in the thresholds to reach each grade by one percentage point. - SCH
4. I was in between answer choices A and D and eventually put D because I thought that the excess of urate crystals effected the fluidity of the synovial joints which lead to physically degrading the cartilage.
Question:4)
The role of sodium urate crystals in gout is to:
Answer:
A) Act as an inflammatory trigger
Suggested additional answer:
D) Physically abrade the joint cartilage
Reasoning:
The question is asking for the role of sodium urate crystals in Gout; it mentions in the course manual for Chapter 22, under “A. Gout” that the first symptom of gout is usually extreme pain in a joint. It further mentions that crystals of sodium urate induce gout when crystals are injected into joints. While causing inflammation would be the major role of urate crystals in gout, I would like to argue that the presence of crystals in the area of a joint known to carry joint cartilage such as the big toe can result in physical abrasion. While I can see what the question is asking for in reference to it’s MAJOR role, I believe that physical abrasion of the joint cartilage leading to extreme pain would carry an important role as well.
I think number 4 The role of sodium urate crystals is: should also be E: causes an autoimmune reaction instead of just A acts as an inflammatory trigger because it specifically says in our notes that the "acute attacks of gout are caused when neutrophils (cells in our body) attack the sodium urate crystals (something made in our body) and initiate inflammation." THis means that the urate crystals cause an autoimmune reaction because they cause neutrophils to attack them and start the inflammation in the first place. I understand that the crystals ARE an inflammatory trigger, but our notes show that they also cause an autoimmune reaction since our own cells are causing the inflammation
Response: The key concept here is that, in inflammatory diseases, the phagocytes damage the tissue while trying to remove the inflammatory trigger. You were advised to think of tissue destruction in gout as being analogous to tissue destruction in periodontitis. Gout is not autoimmune. It would only be called autoimmune if lymphocytes carrying self recognizing T-cell receptors or secreting self recognizing antibodies were involved. Not accepted.
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#5
I understand that answer choice D is correct. I put answer choice B (it is the first enzyme successfully replaced by gene therapy) and I think it should be given credit. On page 7 of chapter 22, it says, “This disease is notable as the first to be successfully treated by human gene therapy. Two patients have been cured of ADA deficiency vitro by the addition of a normal ADA gene, and then reintroduced into the patient.” Since the answer choice B is quite vague, not indicating that it was replaced completely or replaced by a specific enzyme, it made me believe that it was the correct answer. The engineered cells that were put back into the patient, and to me, that means that the enzymes are technically replaced because it is not the original enzymes.
Response: The enzyme replaced to treat this condition is adenosine deaminase (ADA), not ribonucleotide reductase. Although the role of ribonucleotide reductase was given in the manual, the answer was supposed to be accessible by reasoning, not memory. The relevant activity and regulation of ribonucleotide reductase was given in the stem. That the root cause of the condition is the absence of a different enzyme, adenosine deaminase, is given by the name of the condition, adenosine deaminase deficiency. You were supposed to recognize that only one of the options constituted a plausible linkage between those two given pieces of information. That is: failure to dispose of deoxyadenosine would cause it to build up, and when processed to a nucleoside triphosphate it would become one of the inhibitors named in the stem for ribonucleotide reductase. Not accepted.
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Question 16.
This question was poorly worded in my opinion, thus making it tricky. In the question it states that the person “consumes adequate amounts of essential fatty acids.” This made me instantly cross out answer choice E because it says “…there may be a shortage in a particular essential amino acid.” I was amazed that choice E became the answer. I think the question should be thrown out altogether.
Response: Amino acids and fatty acids are not remotely the same thing. The essential amino acids and fatty acids required in the diet are not interchangeable. Not accepted.
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#20
Answer choice on key: D
Additional desired answer choice: E
Type 2 diabetes, as I understood from the manual/lectures, is characterized by severe resistance to insulin. However, the vocabulary from answer choice E reflects a complete stop of insulin production altogether as it reads "eventual LOSS of insulin secretion." I believe this to be the final result of Type 1 diabetes, after beta cells are destroyed.
Response: It is true that insulin resistance is the hallmark of type II diabetes. In the prediabetic state, the insulin resistance is offset by increased production of insulin. Eventually the pancreatic cells are damaged, insulin secretion declines, and glucose levels rise out of control. In contrast, type I diabetes features loss of insulin production without insulin resistance. The most common form of adult onset type I diabetes is due to an autoimmune attack on the pancreatic cells. Hence, this is clearly the false option. Not accepted.
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#22
This question is very vague, ambiguous, and tricky. The question made me believe that the answer should have been facilitated diffusion. On page 7 in chapter 26, it says, “Most ionized metabolites do not readily penetrate cell membranes. They are transported across membranes by specific proteins called translocators or permease by a process called facilitated diffusion.” “Metabolites may be transported across a membrane against a concentration gradient. Such a process, called active transport, requires energy, generally in the form of ATP, and a transport protein.” I don’t think the amount of information given in the manual was enough to answer this particular question. There was no indication of ATP or going against a concentration gradient for the answer to be active transport. I think the best answer choice should have been facilitated diffusion, which is not there. Therefore I think the question should be thrown out.
22. The questions did NOT mention anything about ATP usage so eliminated “A. active transport” as an answer choice because there wasn’t any mention of ATP usage in the question. I didn’t really like any of the answer choices but picked “C. Antiport”
22. A membrane component allows glucose to pass, but only if accompanied by a Na+ ion. This is an example of ______.
A.active transport
B.Passive transport
C. Antiport
D. Membrane Signaling
E. Living cells violating the laws of thermodynamics
Answer on key: A
I believe that credit should also be given for answer choice 'C'. I do not believe the question provided enough information for an answer to be inferred. The question did not state whether the Na+ and glucose would be moving in the same direction, opposite directions, or with/against the cells concentration gradient. I selected answer choice 'C' because the antiport mechanism is a form of active transport and I felt it the possible the substances were being pumped in opposite directions.Thank you!
22. The question states that a membrane component allows glucose to pass but only if accompanied by a Na atom. The question does not state there was any use of energy to make this transfer of glucose into the cell, but rather Na is going down its concentration gradient and bringing in glucose. Therefore, it uses a membrane protein but does not require energy and is a passive transporter not active.
Question:
22) A membrane component allows glucose to pass, but only if accompanied by a Na+ ion. This is an example of:
Answer:
A) Active transport
Suggested additional answer:
B) Passive transport
Reasoning:
It doesn’t mention in the question that ATP was being utilized or that there is a membrane gradient present (therefore requiring ATP to act against it). One of the hallmarks of active transport is that “active transport requires energy, generally in the form of ATP” (from course manual, Chapter 26, “D. Properties of Membranes”). As the question more accurately describes symport, without understanding that energy is required to generate the act of transport, passive transport (also known as facilitated diffusion) appears to be the more appropriate answer.
Response: You were supposed to understand that the Na+/K+ ATPase sets up a Na+ gradient with Na+ higher outside the cells and K+ higher inside, and that the energy represented these gradientsis then be used to pump other molecules against their gradients by requiring Na+ or K+ to pass at the same time. This is active transport, ultimately driven by the utilization of ATP by the Na+/K+ ATPase. In this case, the glucose and Na+ pass in the same direction, so it's called "symport".
If the transporter had required K+ to exit in exchange for glucose entering the cell, that would have been "antiport".
My review notes prior to this exam only listed two membrane functions I said I might test by name. This was one of them. Not accepted.
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29. I did not think that any hormone activity pathways had heterotrimeric G proteins and therefore could not be the answer???
#29
The answer choice reads "Hetero-trimeric G protein." Vocabulary from lecture slide (attached) reads "Trimeric G Protein." I'd made the distinction in my notes, and understood them to be different proteins.
Response. We went over the equivalence of these two expressions in class, with an example from the literature. This challenge is not accepted.
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30. The problem says that the over stimulation of the thyroid glad is the ONLY abnormality which means thyroxin should be at high level and the thyroid glad is overstimulated so TSH should be high as well. The wording makes this question sound like the thyroid is being over stimulated by an abnormal amount of TSH. The answer should be B.
Response. TSH does not come from the thyroid gland. So, this cannot be the answer. A direct clue was given in the mentioning of Graves disease, which was discussed once in class and twice in review sessions. This challenge is not accepted.
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#31 [One of multiple challenges stating that number 31 does not have any correct answer because of the lecture slide stating that norepinephrine is used as a neurotransmitter, and is therefore paracrine]
I am here to challenge number 31 of the biochem exam final and it says “ Which one of the following hormones is water soluble and endocrine?”
Reasons why I believe none of these answers are a right choice:
A)Prostaglandin E1- This is an eicosanoid and therefore is not an endocrine hormone, it is a paracrine hormone. This eliminates it as an answer.
B)Thromboxane- Same explanation as answer A.
C)Thyroxine- thyroxine is endocrine, but not water soluble since it is considered a thyroid hormone, and we know thyroid hormones are lipid soluble.
D) Norepinephrine- This is said to be the right answer on the key, however, it is NOT CORRECT because norepinephrine (according to slide number 2 of the hormones powerpoint that I have attached so you can see), is listed as a PARACRINE HORMONE. This would make this answer incorrect.
E) Cortisol- is lipid soluble and therefore would be wrong.
Therefore, based on these explanations, number 31 does not have a correct answer and should be given credit for. Thank you!
Response. Norepinephrine is both paracrine and endocrine. But, I see how one might be relatively well informed and miss this one. So, I will give credit for all answers to question 31.
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44. In the area that bone resorption is taking place the type I collagen fibers are completely dissolved by acids then completely new fibers are secreted so I did not feel there was a good answer choice at all for this question???
Response: Dissolution of collagen fibers requires matrix metalloproteases (MMPs) also known as collagenases. Not accepted.
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Question 46 should be thrown out. In the lecture "Systemic Control of Bone", Dr. Steffenson emphasizes that thermally-induced isomerization produces Vitamin D3 in the skin. This renders none of the answer combinations correct.
Response: I, II, and III are correct statements. Answer c. II and III is the correct answer. Statement I (which the challenge correctly notes is a true statement) only appears paired with IV, which is incorrect. [I acknowledge that it is an unconventional form of a multiple/multiple question to not have an option that encompasses all the true statements. However, I don't truly believe that should have impeded students from recognizing that c. II and III was a correct answer, hence the question will not be regraded. I believe that any student truly confused by this is adequately compensated by the two point difficulty adjustment applied to the exam. - SCH]
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#48:
A should also be correct.
Justification:
There was nothing in the conference, supplemental reading, or lecture slides mentioning that ameloblasts have high levels of enzyme-rich lysosomes during the maturation phase of enamel formation, something unique to osteoclasts and NOT shared by the ameloblasts.
Response: I (SCH) am triaging challenges to Dr. Steffensen's questions, because he is out of the country. I had no problem finding this information in Dr. Steffensen's slides. Not accepted.
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#58:
B should also be correct.
Justification:
While answer is E is true that everyone has protooncogenes in their genome, being informed of "several" of them would indicate a higher susceptibility to cancer than say, a "normal" amount of protooncogenes. In short, the question was written vaguely because you cannot discern whether "several protooncogenes" is any more than an average person in the question, so choices E and B would make sense given the wording of the question.
58. In the notes it states "it takes a series of mutations to convert a normal cell to a cancerous cell. These are mostly acquired as somatic mutations, although it is possible to inherit one of these mutations as a genetic susceptibility to cancer". I took this as it takes mutations to cause a normal gene or protooncogenes to be converted to a oncogene. And a person with these protooncogenes are more susceptible to mutations that manifest into oncogenes. In addition, there are genes known to cause susceptibility to cancer.
Question:
58) If you are informed that you have several proto-oncogenes in your genome, what does that mean about your state of health?
Answer:
E) Nothing; everyone has proto-oncogenes in their genome.
Suggested additional answer:
C) You have an unusual susceptibility to cancer.
Reasoning:
From the lecture on Chapter 11 – DNA Structure and Synthesis, it Is stated that proto-oncogenes must be mutated into oncogenes for cancer to occur. Hence these, are gain-of-function mutations. While it is true that everyone does have proto-oncogenes in their genome, due to many of the to be thought to be involved in regulating the normal growth of cells (course manual, Chapter 11, “ X. Mutations in DNA and Cancer.”), being informed that you have several proto-oncogenes in your genome (and not specifying whether they were aberrant proto-oncogenes or those typified in most “wild-type” human beings) would also enhance the case that you are more pre-disposed to developing cancer.
Response: Protooncogenes are the normal growth control genes that everyone has. Hence having them means nothing untoward about your health. These genes are essential for normal development. These genes have the property that a mutation can cause them to become overactive and stimulate uncontrolled growth, leading to cancer. If you had an "aberrant" version, as one of the challenges posits, it would no longer be a protooncogene. That would be an oncogene. You would expect to find oncogenes in cancer cells, not in your germline genome. Not accepted.
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Question 60 is worded confusingly and the answer A should be accepted. In lecture we were taught that prokaryotes cannot splice introns. So I interpreted the answer as, it would be impossible to express the correct proteins if the parasitic DNA that was cloned into the E. coli had introns due to the inability of E. coli to process introns.
Question 60: A parasite infecting humans is undergoing characterization. What must be true in order to arrange to express the parasite proteins in E. coli using the same methods as for human proteins?
Answer key: E – The parasite and E. coli must use the same genetic code
I want to challenge for answer B- the parasite and E. coli must use the same transcription factors. First of all, the universal characteristic of genetic code is indicated in the manual: “Until recently, the genetic code was thought to be used identically in all living organisms. However, now that DNA sequences have been compared to protein sequences from many different sources, it is apparent that there are a few minor variations, particularly involving stop codons, in mitochondrial DNA and in a few other organisms.” As what I remember from the lecture, anything with very little exception and not be mentioned in the problem then we should not be overthinking. That was one of the factor that I cross choice E right at the beginning since it was a very few minor exception for the Universal rule of genetic code and the question did not mention anything about consider that minor change. Secondly, in order for a human cDNA clone to express a human protein in E. coli cells, it has to be “properly configured with bacterial transcription and translation control sequences” (according to final exam 2010). Therefore, transcription factors also involve in controlling transcription and translation process.
Response: The phrase "using the same methods as for human proteins" should have made this question a give-away. Since human proteins are expressed in E. coli even though humans have introns, so could parasite proteins. (The technique is to isolate the gene as a cDNA). Since the absence of shared transcription factors is not a problem in expressing human proteins, so it should not be a problem for parasite genes. (The technique is to provide a bacterial promoter, as the challenge noted). Since human nuclear genes and E. coli use the same genetic code, there is nothing in the methods to express human proteins in E. coli that would deal with a parasitic gene encoded by a different genetic code. Hence that would require doing something different than expressing human genes in E. coli (you'd basically have to resynthesize the gene with different codons). Not accepted.