Hi all,
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The pyramidal decussation takes place at the caudal medulla, hence I said that CST lesion in the spinal cord is for all practical purposes always ipsilateral. The mechanism of injury in most spinal flexion/extension injuries (diving, whiplash, falling on one's head from a ladder) is injury to the cervical cord because it is contained in the most mobile part of the spine. You don't need histology here, you need gross anatomy to identify various sections, which is pretty important in neuroanatomy. The brainstem is usually identified by the presence of the various nuclei, peduncles and the the dorsal location of the spinal canal (apart from the distinctive shape of certain levels). The spinal cord can be identified by the expansion of the central grey matter especially at the cervical and lumbar levels, and the typical formation of posterior and anterior horns with a more central spinal canal. For it to be upper and lower motor deficit, you're right it has to be high up, i.e. between C1-c5 (after which the brachial plexus begins and some nerves branch off). A medullary lesion is highly unlikely due to mechanical injury. Vascular lesions or even mass effect will affect more than just the corticospinal tract in the medulla, and such signs will be mentioned (especially on the exam). Here is a link that you might find helpful with regards to gross neuroanatomy.
Thanks for your help! I tend to think of an asterixus/high ammonia type of picture for hepatic encephalopathy…can you clarify the link between hepatic encephalopathy and cerebral edema for me?
Thanks again
4) Do you form immunity against chlamydia? I didn't think you did. There was a stats question where you screened freshman girls for chlamydia and 500 out of 2500 tested positive. Then a year later you tested them again and there were an additional 200 positives, and it then wants you to find the incidence. I thought you would divide 200/2500 as it's a year later and one of the original 500 girls could have been infected again. The correct answer is 200/2000 as you subtract the original 500 girls from the population, so I'm assuming there is immunity? And even if you do have immunity, there are multiple types of chlamydia (D-K), so what if an original girl was infected with D strain and then a year later with F strain? This question seems flawed to me.
What if the girls weren't treated after being screened? I haven't seen the question so I don't know what it says exactly.
It does say that an additional 200 were infected, but that should mean you remove the original 500. The correct answer was 200/2000, and I don't agree with this.
Incidence is new cases per defined time period / total susceptible population. If the 200 additional cases occurred within the same year, then it would be 700/2500. The question said that this was a year later though, so you're beginning with the same 2500 girls again. Whether they are immune should not matter, as there are other serotypes to be infected with, and I don't think it's correct to take those 500 original girls out of the equation because they could be reinfected with chlamydia.
Answers in quote.
Good point. I couldn't find a solid connection on wiki, but I found an article with a couple of theories (link and abstract below). In any case, hepatic encephalopathy and cerebral edema are two SEPARATE diagnostic criteria for Reye's (in varying stages), even though the former probably directly or indirectly leads to the latter.
http://www.ncbi.nlm.nih.gov/pubmed/18688582
"Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited."
I just took NBME 16 and I got this golgi trafficking question wrong by picking D (increased smooth endoplasmic reticulum) I think that its C, due to backing up of proteins in the RER -> dilation - problem with COPII. What do you think?
Yea bad question, but nevertheless, I need to understand something: would getting infected with a different serotype of Chlamydia be the same as getting infected with antigenically shifted Influenza A? I know that shift causes resistance to treatment, whereas different serotypes are usually susceptible to the same treatment (at least for chlamydia, but not sure about other organisms), so then people who get infected with one strain of influenza A are still susceptible to re-infection with another strain that would require different treatment (i.e. a new vaccine), and therefore would be considered among the population of 'new infections' for calculation of incidence. But people who are chronically infected with chlamydia (different serotypes) would probably not be considered 'newly infected'. Just want to clarify this. Have yet to see an incidence question related to antigenic shift...probably because its not as big a deal as I'm making it, or something, I dunnoIt does say that an additional 200 were infected, but that should mean you remove the original 500. The correct answer was 200/2000, and I don't agree with this.
Incidence is new cases per defined time period / total susceptible population. If the 200 additional cases occurred within the same year, then it would be 700/2500. The question said that this was a year later though, so you're beginning with the same 2500 girls again. Whether they are immune should not matter, as there are other serotypes to be infected with, and I don't think it's correct to take those 500 original girls out of the equation because they could be reinfected with chlamydia.
For those who don't mind posting it, what was your # of incorrects and predicted 3 digit score?
can someone please help me settle this? test in <1 week now.
1. went through this forum and usmleforums and couldn't find a thorough or RIGHT answer on the q about the vocal cord position during swallowing, immed after laryngeal irritation, and coughing. i put closed open open and it was wrong but yet that's what the other forum said was right. someone on this thread wrote that they'd be CLOSED after laryngeal irritation, that doesn't make sense to me b/c wouldn't that trap the food in the wrong tube?
2. 20 yr old man that has been heavily drinking all weekend and took three doses of acetaminophen mon. morning at the onset of a severe headache. Increased risk of liver injury b/c of which of the following actions of ethanol?
(chronic alcohol is a p450 inducer but acute alcohol is a inhibitor and he seems like he binged so wtf...)
C. increased bioavailabily of acetaminophen
D.induction of p450 that activate acetaminophen to a hepatotoxic metabolite
E. Met. acidosis due to increased ratio of Nadh/Nad ratio.
3. 15 yr old female ingested Vit D in a suicide attempt. Follow up 1 month later show Ca [C] 10.4 (slightly elevated) What is the mechanism of increased Ca.
A. Decreased Excretion of Ca from GIT
B.Decreased osteoclast activity in bone
C.Increased absorption of ca in GIT
D.Increased 1 Hydroxylase activity in kidney
E.Increased Ostoblast activity in bone
ok so online forums say C which is kinda like duh, that's the MOA of vit d but i don't get why this would still be true a whole month later...wouldn't calcitonin have kicked in? How did you guys know that it was just basically asking the MOA of vit d and not get tripped up on the "1 month" thing?
Thanks in advance guys!!
I know it doesn't meet the criteria for chronic alcohol use, but I assumed that they wanted us to know that chronic use of alcohol induces the p450 metabolism of acetaminophen. I agree, poor question amongst many other poor questions. Just the name of the game with the NBME.
3-12; I was thinking along the same lines and I chose D- increased SER and it was wrongAnswers in quote.
3-12; I was thinking along the same lines and I chose D- increased SER and it was wrong
Gender is better than smoking, I guess. I put gender and it wasn't in my incorrects. I'm assuming you annotated the smoking risk factor thing from a UWorld Q, and I think that list of risk factors in UWorld is referring to risk factors among women.
Unfortunately, it's just one of those "this is a better answer than that" things, even if they're both very good.
Classic osteoporosis, so gender.
Man who develops a temperature after running a 10-km race. The man temperature is going to return back to normal due to which of the following mechanisms?
a. central vasodialation
b. evap of sweat
c. increased minute ventilation
d. increased muscle tone
e. peripheral arteriolar vasoconstriction
f. peripheral venous vasoconstriction
I kind of feel like this question stunk, but what is the biggest risk factor for pancreatic adenocarcinoma? Everywhere I look either just states all of the risk factors or gives conflicting info. I put down diabetes (which is wrong), so I am guessing it has to be smoking? Other choices were obesity, gallstone disease, and hypercalcemia. Thanks!
Dumb question, but there was a question where a blood in the stool test was going to replace colonscopy in order to detect colon cancer, but the doctor had a problem with doing that test. Is it because it has low sensitivity for detecting colon cancer? I put low specificity, just because I thought that many things can cause bleeding. But at the same time, it might not be very sensitive. Anyone know the answer to this one?
2) An animal study is conducted to assess the effects of smoking on pulmonary defense and maintenance mechanisms. For 1 week, normal
male rats are exposed to levels of cigarette smoke comparable to those encountered by humans who smoke cigarettes. Results of
pulmonary testing are compared with baseline levels obtained the week before the smoke exposure. Which of the following sets of changes
is most likely to be observed? Is everything low? smoking impairs mucocilliary clearance I know that much..
Mucus Production and Secretion up/down
Alveolar Macrophage Function up/down
Activity of Airway Cilia up/down
numero 2. should definitely be
Mucus Production and Secretion up
in response to cigarette smoke, combustible fumes and etc mucus production always increases. Just think of the reid index in chronic bronchitis, the submucosal mucous glands increase in size in response to cigarette smoke because they are secreting more mucous in order to clear all those nasty inhaled carcinogens
Alveolar Macrophage Function up
the inhaled carcinogens from cigarette smoke damage the lining of the alveoli. in response to this alveolar macrophages aggregate to clear up the mess
Activity of Airway Cilia down
this one should be easy. carcinogens in cigarette smoke destroy cilia cells lining the airway.
Listen to Dr. Sattar's lecture starting with obstructive pulmonary diseases. he explains all this really well. hope this helped
So up/down/up (mucus, cilia, macrophage) is not an option....someone suggested that it is all down but no one confirmed...do you (or anyone else) know what the correct ways the arrows should be going? Thanks!
***EDIT ...looks like it's supposed to be mucus up and cilia & macrophages both down
Can anyone explain? guess i am confused that the initially wouldn't the cilia and macrophages be going nuts to try and clear whatever the cigarette smoke is causing to accumulate?
2) Are you sure you copied the wording of this question down right? The disease prevalence in heterozygous females would be zero because it's XR, not XD, but if you mean what is the diseased allele prevalence, then the carrier frequency would be 2pq, where p~1 because q=1E-5 (1/100,000) and p+q=1. So 2 x 1 x 1E-5 = 2E-5 = 1/50,000 = B.
What was the gist of the question? It has been removed from the OP.
Right. Since this is XR, the prevalence of affected males gives you q for the male population. This because males can only either be p or q (their Y chromosome is noncontributory). Remember that this same allele, however, also exists in the general population, and so q is the same even for females. In XR disorders, the frequency genotype of the male is equal to the diseased allele prevalence.
Now for females, the allele distribution is (p+q)^2 since females can be homozygous or heterozygous. So we have p^2 as homozygous dominant, q^2 as homozygous recessive (exceedingly rare) and 2pq as heterozygous.
The assumption we make is that given the rarity of the disease, p>>q, and p~1.
So with p~1 and q=1/100000, the heterozygous frequency becomes 2pq = 2/100000 = 1/50000.
If you want to look at it with very fuzzy logic, think of it this way. Homozygous recessive females are too rare to be considered in our equation (think about it, if a single diseased allele appears at a frequency of 1/100000, then the chance of both, by probability is the square of that number, which for all practical purposes is ~0). Hence all diseased males can be thought to have been born of heterozygous mothers. Given that the mother has 50% chance of passing down her recessive gene, there must be twice as many mothers, i.e. 1/50000. I strongly urge that you understand it based on the Hardy Weinberg equilibrium though.
The difference between XR and AR is that in AR diseases, the diseased frequency is q^2 even in males.
I just took NBME 16 and I got this golgi trafficking question wrong by picking D (increased smooth endoplasmic reticulum) I think that its C, due to backing up of proteins in the RER -> dilation - problem with COPII. What do you think?
I cell disease is dilation so C is correct for this this question
thanks. very good explainationAnswers in quote!
Answers in quote.
I think I'm missing something on one of the questions here
The one with the drug experiment where you have blood pressure before and after drug injection
angiotensin II
Drug X
angiotensin II + Drug X
options are aldosterone receptor antagonist
angiotensin II converting enzyme inhibitor (wrong)
angiontensinogen inhibitor
partial agonist at angiotensin II receptors
renin inhibitor
I guess I'm just not seeing something. Why would my choice be wrong? The blood pressure went up a little bit...was it a partial agonist?
You may be correct
on the other hand, I took step 1 back in June and got a 239 on it, which I was quite happy with, and no longer care But hopefully you're helping out someone else who has trouble with that question.
It's A. Cant explain it well though.
Hi everyone, all the comments have been super helpful so far! I have a few Q of my own.
1) Young man with left flank pain radiating to groin; tenderness in left flank and LLQ abdomen; mildly hypoactive bowel sounds and negative occult blood in stool.
I know the answer was speculated briefly above, but I was wondering if anyone knows the answer for sure. I narrowed it down to ureteral calculus and renal infarction (other choices being colon cancer, diverticulitis, epididymitis, torsion of testis - which none of this sounded like).
2) Old man who came in with difficulty sleeping since his wife's death 8 months ago. Wakes up early, cries thinking about her, etc; but still enjoys life with grandkids, remains active in community, etc. No suicidal ideation. Initial action?
Regular appt's to monitor patient
Neuropsych test
Sleep study
Antidepressant
Is it the first one? This patient doesn't quite sound like he has major depressive disorder...
3) Question about a man who has bullous pemphigoid: production of autoantibodies against which structure is causing sx?
Bullous pemphigoid antigen
Collagen type 7
Cystokeratin
Desmoplakin
Plakoglobin
Is the answer really obvious as "bullous pemphigoid antigen"? I thought collagen VII, desmoplakin, and plakoglobin were also components of desmosomes.
4) Middle aged man with 2 months of diarrhea and abd pain that's relieved temporarily with eating and antacids. Serum gastrin is 500 (normal 100) and gastric acid secretion is 80 (6-40). Most definitive treatment to decrease risk of complications?
Low protein diet
Antibiotics
Antihistamine
Section the vagus n to stomach
Surgically remove suspected tumor
I thought it was gastric ulcer caused by H pylori, but antibiotics wasn't correct
I don't think anybody has answered 1-33 yet. I got it right, and I think it's Charcot-Marie-Tooth disease (defective production of myelin and associated with scoliosis, foot deformities -- it says high or flat arches in FA, but I remember learning "hammer toes" as a buzzword). I can't remember what the exact answer options are, but I put down something to do with defective myelin (probably the Schwann cells that you mentioned).
Also, maybe this is a basic/obvious question because nobody seems to have asked about it yet, but I can't figure out the woman with anemia:
2-14: 38 yo woman comes to physician for pre-employment exam; she has no history of serious illness; she takes no meds; her vitals are normal; PE shows no abnormalities
Lab studies show: Hb 8.2, Hct 25%, MCV 69, leukocytes 5900, retic 0.8%, platelets 350K
Most likely DX = ?
Aplastic anemia
Iron-deficiency
Sickle cell
B-thal minor
B12 deficiency
So I was between iron deficiency and B-thal minor, and went with B-thal because people are usually asymptomatic and it was wrong; what am I missing here??