NBME 16 help

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

shubz123

New Member
10+ Year Member
Joined
Sep 10, 2012
Messages
1
Reaction score
0
Hi all,

Members don't see this ad.
 
Last edited by a moderator:
Abnormal origins of multiple renal arteries to each kidney.....

As the kidneys normally ascend in the embryo, so do the origin of the renal arteries. In patients with a horseshoe kidney it gets stuck below the IMA and it cannot ascend so there are two possibilities: Either a low implantation of the renal arteries or the formation of multiple renal arteries. It is a detail for the surgeon to consider when operating an AAA.
 
  • Like
Reactions: 1 user
Can anybody tell me what's the order of importance for these aspects as risk factors for a polyp progression to colorectal cancer?: Sessile growth, villous histology and diameter > 2cm.... thanks
 
Members don't see this ad :)
I actually put "Contemplation" and this question wasn't in my incorrect's. Precontemplation would be if he denied there was even a problem...so I suppose since he's saying he knows something's wrong but isn't ready for change, it's Contemplation.



1. Gastrin. They wanted your thought process to be: Gastritis + pancreatic mass = Zollinger-Ellison --> Neoplastic cells have an abundance of gastrin.
2. Bacterial endocarditis with Enterococcus. Recall that Enterococcus faecalis is associated with endocarditis post-GU procedures.



Hahaha thanks! Just enjoy helping. :)



Yep, chronic inflammation. I actually think chronic inflammation is defined by the presence of a lymphocytic infiltrate as opposed to neutrophilic/monocytic haha. Like you were thinking the fibrosis also hints towards chronic.

plus hep c's most probable outcome is chronic inf /carrier state
 
Can somebody explain this one: " A 38-year-old woman comes to the physician for a pre-employment exam. No history of serious disease. She takes no medications,
vitals are normal, physical is normal, but blood shows:
Hemoglobin 8.2 g/dL
Hematocrit 25%
Mean corpuscular volume 69
Leukocyte 5900/mm3
Platelet count 350,000/mm3
Which of the following is correct?
a-Aplastic anemia ( that what I've chosen, and it was wrong)
b-Iron deficiency
c-Sickle cell anemia
d-Betta-Thalasemia
e-Vit B12 deficiency

If it is not aplastic, then it can't be Vit B12, no Sickle cell. Thus we left with Iron Deficiency and Thalassemia, which are both Microcytic, and... I am stuck here. Thanks for any clarification on this matter
 
Can somebody explain this one: " A 38-year-old woman comes to the physician for a pre-employment exam. No history of serious disease. She takes no medications,
vitals are normal, physical is normal, but blood shows:
Hemoglobin 8.2 g/dL
Hematocrit 25%
Mean corpuscular volume 69
Leukocyte 5900/mm3
Platelet count 350,000/mm3
Which of the following is correct?
a-Aplastic anemia ( that what I've chosen, and it was wrong)
b-Iron deficiency
c-Sickle cell anemia
d-Betta-Thalasemia
e-Vit B12 deficiency

If it is not aplastic, then it can't be Vit B12, no Sickle cell. Thus we left with Iron Deficiency and Thalassemia, which are both Microcytic, and... I am stuck here. Thanks for any clarification on this matter

The differential of a microcytic anemia is essentially iron deficiency vs. thalassemia. If the vignette truly gives no other information than that, then it's iron deficiency; they're testing your knowledge that it's the most common cause. You really only think beta-thalassemia if you have a good reason to (the stem talks about ancestry or hereditary anemia, you're given peripheral smear findings, or a microcytic anemia is refractory to iron therapy).

I want to also make it clear why there's no way this is aplastic anemia: WBCs and platelets are fine. You also really need a good reason to have an aplastic anemia; it's not something people just walk in with for their pre-employment physicals while taking no meds.
 
  • Like
Reactions: 1 user
The differential of a microcytic anemia is essentially iron deficiency vs. thalassemia. If the vignette truly gives no other information than that, then it's iron deficiency; they're testing your knowledge that it's the most common cause. You really only think beta-thalassemia if you have a good reason to (the stem talks about ancestry or hereditary anemia, you're given peripheral smear findings, or a microcytic anemia is refractory to iron therapy).

I want to also make it clear why there's no way this is aplastic anemia: WBCs and platelets are fine. You also really need a good reason to have an aplastic anemia; it's not something people just walk in with for their pre-employment physicals while taking no meds.

Oh, great thinking and reasoning, thank you.
 
  • Like
Reactions: 1 user
I also stumbled on this one:
"75 yo woman with osteopenia on a follow-up examination. Occasional acetaminophen, supplemental Calcium and vit. D. No smoking, drinking and walks 3 miles daily,
BMI 24 kg/m2. Stable wight for 10 years, Pulse-68/min, BP- 124/72 mm Hg. Physical shows no problem.
Labs given to compare Today and 10 years ago:
Serum creatinine 1.o 1.0
Urine creatinine excretion 1000mg/24h 1200 mg/24h
creatinine clearance 64 mL/min 83 mL/min
Which is the most like cause of decreased creatinine clearance rate?
a) High protein diet
b) Over-supplementation with vitD
c) Polycystic kidney disease
d) Renovascular disease
e) Normal aging

And, I went with High-protein diet (don't ask me why, because I still don't know what have possessed me at the moment).
Now, that I thought of it, I think it can't be neither Polycystic disease, no Renovascular, which would come up with hypertension in the question stem.
Hypervitaminosis D has nothing to do with kidney filtration, unless it produces kidney stones, which is not the case.
If creatinine excretion increased, then GFR went up, right? And so did the clearance of creatinine. So, is it Normal aging? I mean what is the concept here?
 
I also stumbled on this one:
"75 yo woman with osteopenia on a follow-up examination. Occasional acetaminophen, supplemental Calcium and vit. D. No smoking, drinking and walks 3 miles daily,
BMI 24 kg/m2. Stable wight for 10 years, Pulse-68/min, BP- 124/72 mm Hg. Physical shows no problem.
Labs given to compare Today and 10 years ago:
Serum creatinine 1.o 1.0
Urine creatinine excretion 1000mg/24h 1200 mg/24h
creatinine clearance 64 mL/min 83 mL/min
Which is the most like cause of decreased creatinine clearance rate?
a) High protein diet
b) Over-supplementation with vitD
c) Polycystic kidney disease
d) Renovascular disease
e) Normal aging

And, I went with High-protein diet (don't ask me why, because I still don't know what have possessed me at the moment).
Now, that I thought of it, I think it can't be neither Polycystic disease, no Renovascular, which would come up with hypertension in the question stem.
Hypervitaminosis D has nothing to do with kidney filtration, unless it produces kidney stones, which is not the case.
If creatinine excretion increased, then GFR went up, right? And so did the clearance of creatinine. So, is it Normal aging? I mean what is the concept here?

I think I recall this one being normal aging -- you're definitely right about none of the others making any sense at all. The decreased creatinine clearance over 10 years is just a loss of nephrons with age, which has been compensated for by angiotensin and aldosterone to prevent serum creatinine from rising overall. I'm not too sure why they would ask this...
 
  • Like
Reactions: 1 users

This is a reminder that posting questions word-for-word or minimally paraphrased is a copyright violation and is against SDN TOS. Please paraphrase questions as much as possible before posting. Posts with full text questions have been deleted.
 
A 23-year-old man comes to the Emergency department because of a 2-week history of back pain refractory to treatment with over-the-counter medications. He demands a prescription for an opioid drig because ''they are the only medications that decrease my pain''. He becomes upset when is told that over-the-counter medications should relieve his symptoms. His temperature is 37.1C, pulse is 70/min, respirations are 18/min, and blood pressure is 120/70mmHg. Physical examination shows no abnormalities. Which of the following is the most appropriate action by the physician?

A) Determine which drugs have been prescribed for the patient in the past
B) Obtain serum toxicology screening on the patient
C) Order an MRI of the spine
D) Prescribe only a 2-week course of a narcotic medication for the patient
E) Refer the patient to a drug addiction program


I put B and I got it wrong. I put B because I think he is a drug abuser, isn't it?? He wants drug and becomes upset!

What is the right answer?
Answer is A i got it right.
 
Sorry for not having the question and answers in front of me as I was pressed for time and didn't screen cap it.

1. Pt. went to Kenya, watery + bloody diarrhea, 12 micrometer trophozoites with erythrophagocytosis. What organism? None of the malarias was an answer choice.
2. Sigmoid colon adenocarcinoma, spreads via which set of lymph nodes?

Sigmoid spreads through inferior mesenterics lymph nodes
 
Bronchial epethelial defect in cystic fibrosis
A) adrenoreceptor
B) Membrane receptor
C) Nuclear rec
D) Protein regulation
E) Protein structure
I put B and got it wrong plz help
 
Members don't see this ad :)
Bronchial epethelial defect in cystic fibrosis
A) adrenoreceptor
B) Membrane receptor
C) Nuclear rec
D) Protein regulation
E) Protein structure
I put B and got it wrong plz help

E) Protein structure (it's a CHANNEL not a receptor)

"here u go plz"
 
The differential of a microcytic anemia is essentially iron deficiency vs. thalassemia. If the vignette truly gives no other information than that, then it's iron deficiency; they're testing your knowledge that it's the most common cause. You really only think beta-thalassemia if you have a good reason to (the stem talks about ancestry or hereditary anemia, you're given peripheral smear findings, or a microcytic anemia is refractory to iron therapy).

I want to also make it clear why there's no way this is aplastic anemia: WBCs and platelets are fine. You also really need a good reason to have an aplastic anemia; it's not something people just walk in with for their pre-employment physicals while taking no meds.

And retic count was fine, IIRC.
 
30. 38 y/o woman seems to have a gastrinoma (serum gastrin concentration is 2000 (normal <100). She also has multiple lipomas and two large non bleeding ulcers. she is started on a proton pump inhibitor. what measurement should you follow?

serum ca
serum cortisol
serum tissue transglutaminase
stool alpha 1 antitrypsin
urine 5hiaa

i probably wouldn't choose 5 hiaa or cortisol. leaning towards calcium


The anwser is Calcium.
 
32. which one of these doesn't have microtubules?
corticol thymocytes
enterocytes in duodenal crypts
erythroblasts in the bone marrow
keratinocytes in stratum basale
ventricular cardiac muscle fibers

i went with ventricular cardiac muscle because it isn't an rapidly dividing cell like the others cells above and got it right!
 

3) 28. 27 y/o with hodgkins gets bone marrow transplant. two weeks after transplant, develops an erythematous, maculopapular rash, diarrhea, and elevated serum liver enzymes and bilirubin. no evidence of infection or drug reaction found. what's the mechanism of these symptoms? It’s graft vs host so answer should be c right?

a-donor macrophages secreting cytokines and affecting host cells

b-donor plasma cells ellaborating antibodies against host cells

c-donor t lymphocytes reacting against host cells

d-host macrophages secreting cytokines and affecting donor cells

e-host plasma cells ellaborating antibodies against donor cells

f-host t lymphocytes reacting against donor cells

I picked F I guess my reasoning was it take 2 weeks for the T lymphocytes to produce antibody against the graft, which is wrong.

Looks like people reasoned out to pick C, but I read from other forum people who picked C still got it wrong. Sometimes the online key is not reliable, so can someone please explain and say the correct answer, thanks
 
3) 28. 27 y/o with hodgkins gets bone marrow transplant. two weeks after transplant, develops an erythematous, maculopapular rash, diarrhea, and elevated serum liver enzymes and bilirubin. no evidence of infection or drug reaction found. what's the mechanism of these symptoms? It’s graft vs host so answer should be c right?
a-donor macrophages secreting cytokines and affecting host cells

b-donor plasma cells ellaborating antibodies against host cells

c-donor t lymphocytes reacting against host cells

d-host macrophages secreting cytokines and affecting donor cells

e-host plasma cells ellaborating antibodies against donor cells

f-host t lymphocytes reacting against donor cells

I picked F I guess my reasoning was it take 2 weeks for the T lymphocytes to produce antibody against the graft, which is wrong.

Looks like people reasoned out to pick C, but I read from other forum people who picked C still got it wrong. Sometimes the online key is not reliable, so can someone please explain and say the correct answer, thanks
GvHD's name gives it away - it's the GRAFT (e.g. donor) reacting against the recipient, so you can automatically rule out D, E, F because the primary source of pathology is not host-derived.

FA says GvHD is due to T-cells proliferating and rejecting host cells (p. 217).
 
  • Like
Reactions: 1 user
section1-1.The study to assess 32 patients in community of 1000 have drug resistant TB during 1-year. after removing them from community to treat,what is the risk for infection with the drug resistant TB next year assuming the risk and susceptibility is constant. 27,29,31,32 (wrong as I picked it),33.

If anyone can help me with little explanation I will appreciate it. I already read all the posts about NBME 16.
 
Last edited:
section1-1.The study to assess 32 patients in community of 1000 have drug resistant TB during 1-year. after removing them from community to treat,what is the risk for infection with the drug resistant TB next year assuming the risk and susceptibility is constant. 27,29,31,32 (wrong as I picked it),33.

If anyone can help me with little explanation I will appreciate it. I already read all the posts about NBME 16.

The answer is 31. The percent of people who get the drug-resistant TB each year is 32/1000. Then since 32 people were taken away, you have 968 people left. So you multiply 968*(32/1000), giving you a number very close to 31. Honestly I feel like the math is pretty tricky on this one so you would probably want to estimate rather than doing all the division and multiplication.
 
  • Like
Reactions: 1 user
Answers in quote.

4-43
Fever, N/V/D. Little urine production past 12 hours. Supine: pulse 92, BP 110/70. Standing: pulse 110, BP 80/60. Dry mucous membranes. WBC 7200. Na 146, Inc urea, creatinine, uric acid. Urine shows no protein, specific gravity of 1.03, no RBC, Na 10, Creatinine 19.
Answers: A. ATN, B. bladder outlet obstruction, C. interstitial nephritis, D. membranous GM, E. volume depletion
I picked A. Could the answer have been E? What distinguishes the two here?

___________________
I also got this question wrong, but for the sake of completion, the way you can also tell it's E is if you calculate the BUN/Cr ratio.

Since BUN/Cr > 20, you know that the problem is pre-renal. That leaves only the choice of dehydration (E) possible, whereas ATN is an intra-renal problem, which would most likely show a ratio <20. I hope I'm making sense here.
 
  • Like
Reactions: 1 user
Only one week out and there's still a handful of stuff I'm still not solid on. I got a 234 which isn't bad but I don't even know where I'm supposed to get some of this information from. I guess I just gotta keep doing questions.
1. 3 year old boy with cough and larva. Is it supposed to be meat products?
2. Guy with pain in big toe and drinking home-brewed alcohol. What is his most likely predisposing factor?
3. Woman with severe headache and eye problems. Where is the aneurysm?
4. Woman with stomach pain and ulcer like systems. Which artery is supposed to be stenosed?
5. How is the pain transmitted in that patient using the capsaicin cream?
6. African American with an itchy face, jaw and neck. Why isn't it rosacea? Is it more likely to be lupus?
7. What increases the pulmonary flow?
8. What is supposed to decrease the old woman's risk of fracture?
9. What will the sputum cultures grow in the homeless person?
10. What is the mechanism of induration in the child who got stung?
11. Why did the 84-year old woman have a worsening clinical course?
12. How is poliovirus translated without a cap?
13. What is the underlying mechanism of Li-Fraumeni?
14. What part of the kidney is first to show anoxic injury?
 
Only one week out and there's still a handful of stuff I'm still not solid on. I got a 234 which isn't bad but I don't even know where I'm supposed to get some of this information from. I guess I just gotta keep doing questions.
1. 3 year old boy with cough and larva. Is it supposed to be meat products?
Don't recall
2. Guy with pain in big toe and drinking home-brewed alcohol. What is his most likely predisposing factor?
Drinking alcohol leading to gout
3. Woman with severe headache and eye problems. Where is the aneurysm?
Don't recall. Posterior communicating maybe?
4. Woman with stomach pain and ulcer like systems. Which artery is supposed to be stenosed?
Don't recall
5. How is the pain transmitted in that patient using the capsaicin cream?
Substance P I think?
6. African American with an itchy face, jaw and neck. Why isn't it rosacea? Is it more likely to be lupus?
Pseudofolliculitis barbae
7. What increases the pulmonary flow?
Don't recall
8. What is supposed to decrease the old woman's risk of fracture?
Taking walks, weight bearing exercises
9. What will the sputum cultures grow in the homeless person?
Don't recall. Kleb or some type of anaerobe?
10. What is the mechanism of induration in the child who got stung?
Contraction of myoepithelial cells leading to gaps in endothelium
11. Why did the 84-year old woman have a worsening clinical course?
Don't recall
12. How is poliovirus translated without a cap?
Internal ribosome sequence
13. What is the underlying mechanism of Li-Fraumeni?
Loss of heterozygosity?
14. What part of the kidney is first to show anoxic injury?
PCT
Don't remember the others without the full question.
 
Thanks guys, that cleared some stuff up. It seems obvious now but I don't know why it didn't come to me during the test.

13. What is the underlying mechanism of Li-Fraumeni?
Regulation of apoptosis-- think about this as which answer choice is most likely to cause cancer
Doesn't p53 have some DNA repair function or am I just misremembering?


11. Why did the 84-year old woman have a worsening clinical course?
She broke her leg and they gave her morphine to self medicate with. Afterwards, she came in with symptoms of a morphine overdose. I thought she increased her dose because she was starting to build tolerance but that was wrong apparently.

4. Woman with stomach pain and ulcer like systems. Which artery is supposed to be stenosed?

A woman comes to the physician because of a 1-year history of abdominal pain after meals and weight loss. The pain is relieved when she eats less. She has a history of atherosclerosis and triple bypass. Physical examination shows a soft, nontender abdomen and an abdominal bruit. Pedal pulses are diminished. What artery is stenosed?
A)Greater Hepatic
B)Hepatic
C) Right Gastric (wrong)
D)Superior mesenteric
E) Supraduodenal
 
A woman comes to the physician because of a 1-year history of abdominal pain after meals and weight loss. The pain is relieved when she eats less. She has a history of atherosclerosis and triple bypass. Physical examination shows a soft, nontender abdomen and an abdominal bruit. Pedal pulses are diminished. What artery is stenosed?
A)Greater Hepatic
B)Hepatic
C) Right Gastric (wrong)
D)Superior mesenteric
E) Supraduodenal
No ulcer. All the physical findings point to atherosclerosis of the SMA.
 
Only one week out and there's still a handful of stuff I'm still not solid on. I got a 234 which isn't bad but I don't even know where I'm supposed to get some of this information from. I guess I just gotta keep doing questions.
1. 3 year old boy with cough and larva. Is it supposed to be meat products?
Feces- contaminated soil (fecal oral)
9. What will the sputum cultures grow in the homeless person?
Normal oral flora (aspiration)
11. Why did the 84-year old woman have a worsening clinical course?
Morphine is metabolized to active metabolites that accumulate
12. How is poliovirus translated without a cap?
Presence of an internal ribosome entry site
 
Sorry if I reposted this question, tried searching but couldn't find it. Few days before my exam so it may be my impatience settling in lol but

44 yo man, 2 months of ab. pain/diarrhea temporarily relieved after eating + antacids. Lab shows serum [gastrin] = 500 (N=50-100) and gastric acid secretion is 80 mEq/h (N=6-40). Which is most definitive tx at this time to decrease pt's risk for complications?

A) low protein diet
B) oral antibiotic
C) oral antihistamine
D) vagotomy
E) surgical removal of suspected tumor

So I picked B (wrong) because I thought it would be more likely for him to have ↑ gastrin levels d/t his use of antacids/H. pylori vs. a neoplasm as rare as gastrinoma. Also on top of the fact that his pain was relieved BY antacids (I always thought gastrinoma sx were unresponsive to anti-H+ therapy). I'm guessing the answer is E? If so, is 500 pg/mL gastrin level typical for a gastrin-secreting tumor and so if we see gastrin levels like that on Step, we automatically assume gastrinoma?
 
Not sure if brought up already, but there was a renal physio question regarding the addition of 100% nitrogen gas via a mask to animal subjects, and they wanted to know which part of the kidney would suffer from hypoxia first

Answers were things like bowmans capsule, glomerulus, efferent arteriole, DCT, PCT. I honestly wasn't sure, I know the medulla is the first to get hypoxic but I wasn't sure how to use that information to answer this question.
 
Not sure if brought up already, but there was a renal physio question regarding the addition of 100% nitrogen gas via a mask to animal subjects, and they wanted to know which part of the kidney would suffer from hypoxia first

Answers were things like bowmans capsule, glomerulus, efferent arteriole, DCT, PCT. I honestly wasn't sure, I know the medulla is the first to get hypoxic but I wasn't sure how to use that information to answer this question.
PCT. You need a bunch of ATP for all that active transport that goes on there.
 
  • Like
Reactions: 1 user
Alright one more. Another question referred to an image of an anus (highly memorable) that has a raised lesion on the anus, and a majority of it was black in color. What type of lesion was it? I remember seeing the exact same thing on either UWorld or NBME 15.

cadidiasis, lymph obstruction, venous HTN, VZV, tinea cruris were some options
 
Alright one more. Another question referred to an image of an anus (highly memorable) that has a raised lesion on the anus, and a majority of it was black in color. What type of lesion was it? I remember seeing the exact same thing on either UWorld or NBME 15.

cadidiasis, lymph obstruction, venous HTN, VZV, tinea cruris were some options
I think it was a hemorrhoid. Venous HTN.
 
  • Like
Reactions: 2 users
A 62-year-old man with unstable angina pectoris undergoes coronary catheterization. In order to visualize the anterior interventricular (left anterior descending) artery, the tip of the angiographic catheter would need to be placed into the orifice of which of the following arteries?:

A) Circumflex
B) Left coronary
C) Left marginal
D) Right coronary
E) Right marginal

I put A and I got it wrong. What is the correct answer?

I think it is so specific! I don't do angioplastic everyday. Damn!
I put Left Coronary and got it correct.
 
  • Like
Reactions: 1 user
3-12
4 mo boy has auto recessive skeletal dysplasia with abnormal endochondral bone formation. Null mutations in gene for protein that controls traffic of vesicles to golgi. EM shows?
Answers: A. dec RER, B. dec SER, C. dilated RER, D. inc SER, E. large lysosomes, F. small lysosomes
I thought just based on golgi, it would either be backwards (RER) or forward (vesicles). I picked E. I'm guessing the answer is D then, but I don't know how you can reason the correct answer between the two.


A long time has passed since this thread was posted but people are still looking for these answers and I found the definite one for this stupid question.

"Achondrogenesis type 1A is caused by a defect in the microtubules of the Golgi apparatus. In mice, a nonsense mutation in the thyroid hormone receptor interactor 11 gene (Trip11), which encodes the Golgi microtubule-associated protein 210 (GMAP-210), resulted in defects similar to the human disease. When their DNA was sequenced, human patients with achondrogenesis type 1A also had loss-of-function mutations in GMAP-210. GMAP-210 moves proteins from the endoplasmic reticulum to the Golgi apparatus. Because of the defect, GMAP-210 is not able to move the proteins, and they remain in the endoplasmic reticulum, which swells up."

so it's C for sure, hope this helps someone
 
  • Like
Reactions: 1 users
1. 58 yo African American has CHF, S3, EF=30%,treatment with hydralazine and isosobide dinitrate, which med is contraindicated? I now sildenafil is contraindicated, but why is diltiazem not contraindicated in CHF?
2. Man has severe low back pain radiating down to the left leg, he started weight-lifting regimen, what is responsible for his pain. answer is rupture of the intervetebral disk, why "tear in the sciatic nerve" is not correct? Is it because tearing a nerve is not likely during weight-lifting? What generally tears a nerve? Trauma?
Thanks!
 
1. 58 yo African American has CHF, S3, EF=30%,treatment with hydralazine and isosobide dinitrate, which med is contraindicated? I now sildenafil is contraindicated, but why is diltiazem not contraindicated in CHF?
2. Man has severe low back pain radiating down to the left leg, he started weight-lifting regimen, what is responsible for his pain. answer is rupture of the intervetebral disk, why "tear in the sciatic nerve" is not correct? Is it because tearing a nerve is not likely during weight-lifting? What generally tears a nerve? Trauma?
Thanks!
Have you ever heard of "nerve tearing" as a common cause of anything? That would be an incredibly rare and SEVERE problem, associated with serious loss of function in that limb, not just pain. Everyone and their mother has a ruptured disk though, which impinges on their nerves causing the radiating pain.

Your first question is just a classic association: nitrates + PDE5 inhibitor = life threatening hypotension. Best answer, no questions asked, don't overthink it.
 
2. poliovirus mRNA lacks 5'm7G cap but is translated efficitnetly by cellular ribosomes. which of the following additional structureal features of poliovirus mrna is the most likely cause of its ability to be translated in the absence of a cap?
a. absence of 3' untranslated region (utr)
b. absence of a 5' utr
c. absence of a polyA tail (wrong)
d. presence of an internal ribosome entry site
e. very short open reading frame

Thanks.
D
https://en.wikipedia.org/wiki/Internal_ribosome_entry_site

although this is really one you should be able to get by eliminating the others. It lacks a functioning initiation complex (cap) so it must have another way to interact with the ribosome to be translated. The other choices make no sense as far as a way to initiate translation.
 
  • Like
Reactions: 1 users
Atrophy. By taking thyroxine, she'll cause TSH levels to go down, which will reduce thyroid stimulation.



Kidney or lung, but I would probably go for kidney on this one. He's a smoker, which is a risk factor for both. Hypercalcemia points to PTHrP production by either a squamous cell carcinoma of the lung or a renal cell carcinoma, but the polycythemia points more to renal cell carcinoma since renal cell carcinoma can produce EPO.



Don't remember. I probably said Wegener's, though, because of the nasal and lung involvement and the fact that I think proteinase 3 is in neutrophils, so C-ANCA.




Low sensitivity. For diseases that will kill you quickly if not treated (like colon cancer), you want a more sensitive initial (screening) test.



Syrinx: She has a cape-like distribution of pure sensory impairment.



Increase in width. Lower sample size => Less certainty about where the mean actually lies => wider confidence interval.



Decreased lamellar bodies. Lamellar bodies are secretory organelles. The type II pneumocytes make surfactant, and this infant has respiratory distress syndrome, so they're not secreting as much.



Crescentic => RPGN. Often caused by goodpasture's, which is Abs against basement membrane. It often has lung involvement as well.



Indomethacin closes the PDA by inhibiting production of PGE2, which is an arachidonic derivative and therefore made by Cyclooxygenase (COX). Therefore, COX is the answer.

I know it's not Lung. But 2015 FA says mets to brain are from Lung > breast > prostate > melanoma > GI. So is it prostate?
 
Last edited:
5) 12 year old with walking abnormality for 6 months. mild atrophy and hammer toes.nerve biopsy shows

abnormal myelin sheaths

This is right, but i don't think it's Chacort marie tooth. I think this is friedriechs ataxia
hammer toes is a key word


10) 28 yr old lady w/ 1 month history of pelvic pain that has become increasingly severe during the past week. Her mensrual flow has been unusually heavy during her last three menstrual periods. Menses have occurred at 24-28 day intervals since menarche at the age of 12 years. Phys exam shows a palpable mass in the left adnexa. Serum studies show an increased CA 125 concentration. Vaginal ultrasonography shows an 8 cm mass in the left ovary. During surgical removal of the ovary, which of the following structures passing inferior to the ovary must be protected? I think its ureter but wanna double check w you

external iliac artery, internal iliac artery, ovarian ligament, round ligament of the uterus, ureter
I put ureter too, but I'm also wondering about this one

This is right as well.
Remember the mneumonic. "Water (ureters) under the bridge (uterine artery). In first aid.

the question with diabetic pt taking hydrochlorothiazide whose BP doesn't go down, and what additional drug to use. I would also use an ACE or an ARB, but in this case the pt has renal dz (diabetes and microalbuminuria)

According to FA, ist line for HTN and diabetes is ACEi/ARB, then Ca channel blockers, then diuretics, beta blockers and alpha blockers
Clonidine is very short acting and cause cause severe rebound hypertension when a dose is skipped. so I think its only used in severe hypertensive emergency
 
Top