takethat12

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I got that one wrong too. Google blue vaginal mucosa; it's a marker for pregnancy.
Ultrasound won't reliably pick up the fetus until week . . . well I don't know but way later than hCG. I want to say week 7 or 8.

I hate to perseverate or derail the thread, but doesn't anyone who got right answer remember the question I posted on the last page? The elderly woman with the long chronic condition who dies in the hospital and they show a gross picture of her spine.
 

ipizzy

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4. 29: locate portion of brain which is responsible for decreased touch sensation. not much help without picture
I think some people on here put that it was the somatosensory cortex, but I was wondering if it could have been the region over the parietal lobe? The sensory deficits tested were all things that required integration of sensory information (graphesthesia, two point discrimination), which are lost with parietal lobe lesions.

Anyone get extended feedback and know the correct answer here?
 
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ijn

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Based on the prompt, she has had a "long illness" which you can interpret as chronic disease. Therefore you can assume IL-1, IL-6, and TNF-alpha are elevated relative to the baseline.

IL-1 activates osteoclasts and can accelerate osteoporosis. This can result in femoral head fracture or vertebral collapse. In the image you can see trabecular thinning in the vertebral column, which is a buzz phrse for osteoporosis.

Now you can ask, why can't she have multiple myleoma? It's possible. But keep in mind that the lytic bone lesions in multiple myeloma are also due to elevated IL-1. So the answer wouldn't change. Hypergammaglobulinemia is just a distraction and would be less correct than a cytokine related directly to the pathophysiology of bone reabsorption.
 

ijn

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I think some people on here put that it was the somatosensory cortex, but I was wondering if it could have been the region over the parietal lobe? The sensory deficits tested were all things that required integration of sensory information (graphesthesia, two point discrimination), which are lost with parietal lobe lesions.

Anyone get extended feedback and know the correct answer here?
She has a sensory deficit in her left hand, therefore the answer is the somatosensory cortex on the right hemisphere, answer "B."

If she had a right parietal lobe lesion then you're missing a major presentation in her history - namely hemineglect of her left side. Obviously she can tell she has a problem in her left hand based on the prompt. That would lean me away from parietal lobe problems. Graphesthesia can also occur with any lesion between the DRG and the somatosensory cortex. It's not just a parietal lesion.
 

ipizzy

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She has a sensory deficit in her left hand, therefore the answer is the somatosensory cortex on the right hemisphere, answer "B."

If she had a right parietal lobe lesion then you're missing a major presentation in her history - namely hemineglect of her left side. Obviously she can tell she has a problem in her left hand based on the prompt. That would lean me away from parietal lobe problems. Graphesthesia can also occur with any lesion between the DRG and the somatosensory cortex. It's not just a parietal lesion.
Hmm I see. Is neglect something that occurs with all right parietal lobe lesions (I thought not)? Or is it just too buzzwordy to be wrong here? Thanks for your quick response!
 

ijn

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Hmm I see. Is neglect something that occurs with all right parietal lobe lesions (I thought not)? Or is it just too buzzwordy to be wrong here? Thanks for your quick response!
Somatosensory cortex is part of the parietal cortex, so I guess the first thing to look for is sensory loss and graphesthesia. Maybe the better way to look at it is in terms of large and small parietal strokes.

I think hemineglects are signs of a larger stroke while sensory losses are of a smaller stroke. If they were leading you towards a generalized parietal stroke I'd want to see at least one of the following 1) hemineglect 2) apraxias, 3) gerstmanns (finger agnosia, agrapha/alexia/left and right hand confusion), 4) inferior contralateral homonymous quadrantanopia.
 

ipizzy

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Somatosensory cortex is part of the parietal cortex, so I guess the first thing to look for is sensory loss and graphesthesia. Maybe the better way to look at it is in terms of large and small parietal strokes.

I think hemineglects are signs of a larger stroke while sensory losses are of a smaller stroke. If they were leading you towards a generalized parietal stroke I'd want to see at least one of the following 1) hemineglect 2) apraxias, 3) gerstmanns (finger agnosia, agrapha/alexia/left and right hand confusion), 4) inferior contralateral homonymous quadrantanopia.
Makes sense. Thanks :D
 
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40. A 26-year-old primigravid woman delivers a 2948-g (6-lb 8-oz) male newborn at
term. Six months ago, she received a vaccine, Streptococcus agalactiae (group B),
serotype III, during a clinical trial. Screening indicated that she had generated an
antibody response to this polysaccharide antigen within 1 month of the vaccination.
This antibody was detected in her serum immediately prior to the onset of labor.
Eight hours after delivery, the newborn appears progressively lethargic, and his
temperature is 38.2°C (100.8°F). Cerebrospinal fluid and blood cultures grow S.
agalactiae (group B), serotype III. It is suspected that the mother produced only one
antibody isotype in response to the vaccine. This isotype is most likely which of the
following?
A) IgA
B) IgD
C) IgE
D) IgG (wrong)
E) IgM


I thought that IgG was the only antibody that crossed the placenta? any thoughts?
 

Dr McSexy

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You are right in that IgG is the only Ig type that crosses the placenta.

However, you should re-read the question carefully. Question basically states that the mother formed antibodies, however her baby still got sick. So, that means that she didn't form IgG antibodies, otherwise they would have crossed the placenta and protecting the baby.

So, then it asks which is the most likely type of antibodies that DID form, which is IgM.
 

ijn

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I think the answer is IgM. When you have non-thymic dependent antigens like polysaccharides, you can only get IgG immunity if they're conjugated to proteins like toxoids. Pneumovax works in the same way as this theoretical GBS vaccine. So neither of those vaccines could provide immunity to the child because IgM does not cross the placenta.
 
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wow I thought this test was kind of stupid. I didn't think it was any more difficult than NBME 12, but an uncomfortable amount of questions were ambiguous or poorly worded (with arguable answers for many). I really hope the real test is more straightforward (like the other NBMEs).

Anyway, got a couple questions

1. the anatomy question about which artery supplies the esophagus:

dumb question, but when you do something like an esophagectomy or a splenectomy and they ask which artery needs to be ligated, it's usually the artery supplying the organ right??

2. What do you observe when you infuse EPI and watch b2-receptors?

I get that uterine relaxation is the answer, but don't you also have increased myocardial contractility (or is this just b1) and lipolysis (I KNOW this is b2) with b2? <-- THIS one pissed me off

3. Pseudomonas creating biofilm:

hmm I've really only heard about biofilm in the context of S. epidermis.. should I just assume most nosocomial bugs associated with catheters and such can produce biofilm? And how do we know it didn't get antimicrobial resistance from a bacteriophage?

4. Location of the branchial cleft cyst (anterior to SCM)

wtfff anterior to SCM is pretty much in the midline of the neck, no? I put "posterior to parotid" since that would be pretty darn lateral. Hated this question, knew EXACTLY what I was looking for, but couldn't find it. BS

5. Girl who ODs on metformin. What is the likely lab finding?

Sure I could've gone with the knee-jerk answer and picked "lactic acidosis" but I figured that was a non-dose-dependent adverse effect (I guess it isn't?) and went with "hypoglycemia." Can't metformin OD cause hypoglycemia? I know generally sulfonylureas are associated with hypoglycemia, but I figured ingesting a whole bottle of metformin could do the trick too. guess I should just go with the easy answer :(

6. Picture of the brain and the lady who had seizures (answer was AVM)

Can someone explain this? All I could get from the pic was that it looked like the remnants of liquefactive necrosis and therefore chose the only ischemic brain disease on there (neonatal stroke). what exactly happens in an AVM?

7. Blue-tinged vagina LOL this means preggers??!


thanks all!
 
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I have a few questions from the NBME. I apologize if I have missed the explanation previously in the forum on any of them. Any explanation would really be appreciated :) Thank you SO much!!

A 55 yo man comes to the physician because of two episodes of painless, blood-tinged urine for the past week. His last episode was two days ago. He has smoked 1 pack of cigs daily for 35 years. Vital signs are WNL. PE shows no abnormalities. Urinalysis shows normal findings except for microscopic blood. Which of the following is the most likely diagnosis?
a). Bladder cancer
b). Bladder diverticulum
c). Interstitial cystitis
d). Nephrolithiasis
e). UTI
-I put UTI but looking back on it that was really stupid considering there were not WBC's. But is the right answer bladder cancer? I realize that painless hematuria is bladder cancer until proven otherwise but he's only had it for a week...which really makes me lean towards something else

A 38 yo woman at 32 weeks gestation is brought to the physician because of a two day history of fever, nausea, vomiting, and muscle aches. She appears acutely ill. Her temp is 102.2, pulse is 120/min, and respirations are 20/min. A photomicro of a gram stain of an organism recovered from a blood culture is show. Which of the floowing is the most likely causal organism?
a). Corynebacterium urealyticum (should I have heard of this before?)
b). Gardnerella vaginalis
c). Listeria mono
d). Rhodococcus equi (haven't heard of this one either)
e). Staph aureus

A autopsy is done on a 50 yo man who died of pneumonia despite 5 days of AB therapy in the ICU. He had a 15 year history of alcoholism. A photograph of a sagittal section of the brain is shown. Base on this pathology, which of the following findings was most likely present on neuro exam of the patient prior to his death?
a). Dysdiadochokinesia
b). Dysmetria on finger-nose testing
c). essential tremor
d). gait ataxia
e). Rhomberg
This one was previously discussed and someone mentioned that he was an alcoholic so think gait ataxia. But if I didn't know this association, is there a way to answer the question? How can I rule out the other answers?

A female newborn is delivered at 34 weeks in an advanced-care setting where special delivery systems are available. The dx of a persistent pulmonary HTN is made. Considering that the newborn can be carefully monitored for methemoglobinemia, which of the following is the most appropriate therapy?
a). Desflurane
b). Hyperbaric O2 chamber
c). Nitric oxide
d). Nitrous oxide
e). O2 diluted with He
This question was also previously discussed in the setting of the difference between nitric oxide and nitrous oxide, but why wouldn't you want to use a hyperbaric O2 chamber?

A 50 yo man comes to the physician because of a 2 mo history of pain in his wrists, changes in skin color, and progressive fatigue. His brother had DM2 and cirrhosis. PE shows bronze-colored skin, tenderness of the MCP joints in both hands, and hepatosplenomegaly. Serum studies show:
AST=100
ALT=110
Ferritin=1200
TIBC=200 (N=250-400)
Transferrin sat=80% (N=20-50)
Analysis of a liver bx specimen shows a markedly increase Fe concentration and cirrhosis. Which of the following is the most likely cause of the findings in this patient?
a). Increased EPO action
b). Increased intestinal Fe abs
c). Increased oral Fe intake
d). Decreased EPO
e). Decreased Fe excretion (wrong)
f). Decreased serum tranferrin concentration

A previously healthy 54 yo man comes to the clinic because of lightheadedness for 6 hours. His symptoms began after skiing at a resort at an altitude of 9000 ft. he has been taking a carbonic anhydrase inhibitor since 2 days before arriving at the resort. His BP is 110/60 which sitting and 95/50 while standing. PE shows no other abnormalities. Which of the following is the most likely cause of his orthostatic hypotension?
a). High-alt. sickness
b). Hypovolemia
c). Hypoxia
d). Impaired sympathetic nerve activity (wrong)
e). Respiratory alkalosis
-I can see why some of these would make you lightheaded, but not why any of them would cause orthostatic hypotension

An investigator is studying the human immune response to tumor cell antigens in malignancies. Which of the following sets of cancer types and tumor antigens is most likely to produce the highest AB titer?
a). B-cell lymphoma, CD19
b). Breast cancer, HER2/Neu
c). Cervical cancer, HPV type 16 E6 protein
d). Melanoma, tyrosinase
e). Prostate cancer, prostate acid phosphatase
-This question was discussed before and apparently the correct answer is A (I put B) but I don't have a clue as to why. Any explanation would be greatly appreciated :)
 
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Dr McSexy

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I have a few questions from the NBME. I apologize if I have missed the explanation previously in the forum on any of them. Any explanation would really be appreciated :) Thank you SO much!!

A 55 yo man comes to the physician because of two episodes of painless, blood-tinged urine for the past week. His last episode was two days ago. He has smoked 1 pack of cigs daily for 35 years. Vital signs are WNL. PE shows no abnormalities. Urinalysis shows normal findings except for microscopic blood. Which of the following is the most likely diagnosis?
a). Bladder cancer
b). Bladder diverticulum
c). Interstitial cystitis
d). Nephrolithiasis
e). UTI
-I put UTI but looking back on it that was really stupid considering there were not WBC's. But is the right answer bladder cancer? I realize that painless hematuria is bladder cancer until proven otherwise but he's only had it for a week...which really makes me lean towards something else

It's bladder cancer.

A 38 yo woman at 32 weeks gestation is brought to the physician because of a two day history of fever, nausea, vomiting, and muscle aches. She appears acutely ill. Her temp is 102.2, pulse is 120/min, and respirations are 20/min. A photomicro of a gram stain of an organism recovered from a blood culture is show. Which of the floowing is the most likely causal organism?
a). Corynebacterium urealyticum (should I have heard of this before?)
b). Gardnerella vaginalis
c). Listeria mono
d). Rhodococcus equi (haven't heard of this one either)
e). Staph aureus

I had never heard of those either. It's Listeria . I thought that this was a BS question, jmo.

A autopsy is done on a 50 yo man who died of pneumonia despite 5 days of AB therapy in the ICU. He had a 15 year history of alcoholism. A photograph of a sagittal section of the brain is shown. Base on this pathology, which of the following findings was most likely present on neuro exam of the patient prior to his death?
a). Dysdiadochokinesia
b). Dysmetria on finger-nose testing
c). essential tremor
d). gait ataxia
e). Rhomberg
This one was previously discussed and someone mentioned that he was an alcoholic so think gait ataxia. But if I didn't know this association, is there a way to answer the question? How can I rule out the other answers?

No clue. Maybe someone else has an answer. I missed this one too... of course, I couldn't even tell the cerebellum was atrophied :laugh: .

A female newborn is delivered at 34 weeks in an advanced-care setting where special delivery systems are available. The dx of a persistent pulmonary HTN is made. Considering that the newborn can be carefully monitored for methemoglobinemia, which of the following is the most appropriate therapy?
a). Desflurane
b). Hyperbaric O2 chamber
c). Nitric oxide
d). Nitrous oxide
e). O2 diluted with He
This question was also previously discussed in the setting of the difference between nitric oxide and nitrous oxide, but why wouldn't you want to use a hyperbaric O2 chamber?

No clue as to why you wouldn't want to use hyperbaric O2 chamber. When the stem mentioned methemoglobinema, I took it as asking if I knew what can cause methemoglobinemia, and went w/ Nitric oxide, due to Nitrates and stuff.

A 50 yo man comes to the physician because of a 2 mo history of pain in his wrists, changes in skin color, and progressive fatigue. His brother had DM2 and cirrhosis. PE shows bronze-colored skin, tenderness of the MCP joints in both hands, and hepatosplenomegaly. Serum studies show:
AST=100
ALT=110
Ferritin=1200
TIBC=200 (N=250-400)
Transferrin sat=80% (N=20-50)
Analysis of a liver bx specimen shows a markedly increase Fe concentration and cirrhosis. Which of the following is the most likely cause of the findings in this patient?
a). Increased EPO action
b). Increased intestinal Fe abs
c). Increased oral Fe intake
d). Decreased EPO
e). Decreased Fe excretion (wrong)
f). Decreased serum tranferrin concentration

increased intestinal Fe abs. Pt has hemochromatosis.

A previously healthy 54 yo man comes to the clinic because of lightheadedness for 6 hours. His symptoms began after skiing at a resort at an altitude of 9000 ft. he has been taking a carbonic anhydrase inhibitor since 2 days before arriving at the resort. His BP is 110/60 which sitting and 95/50 while standing. PE shows no other abnormalities. Which of the following is the most likely cause of his orthostatic hypotension?
a). High-alt. sickness
b). Hypovolemia
c). Hypoxia
d). Impaired sympathetic nerve activity (wrong)
e). Respiratory alkalosis
-I can see why some of these would make you lightheaded, but not why any of them would cause orthostatic hypotension

hypovolemia due to acetazolamide use. Hypovolemia is a pretty common cause of orthostatic hypotension

An investigator is studying the human immune response to tumor cell antigens in malignancies. Which of the following sets of cancer types and tumor antigens is most likely to produce the highest AB titer?
a). B-cell lymphoma, CD19
b). Breast cancer, HER2/Neu
c). Cervical cancer, HPV type 16 E6 protein
d). Melanoma, tyrosinase
e). Prostate cancer, prostate acid phosphatase
-This question was discussed before and apparently the correct answer is A (I put B) but I don't have a clue as to why. Any explanation would be greatly appreciated :)

Answer is actually C. I don't think anyone has come up w/ a great explanation other than that it's the only one of the answer choices that involves a non-self protein
...
 

LRAccord624

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Ok I have a quick question...

60yo male comes to physician bc of 2wk history of fatigue and exercise intolerance. He was diagnosed w/stage I HTN one month ago and began treatment with propranolol. Pulse is 56/min compared to 72/min a month ago. Treatment switched to pindolol; symptoms resolve in a month and pulse is 68/min. What MoA of pindolol explains its affect on the pt's heart rate?
A) Competitive agonism
B) Competitive antagonism
C) Inverse agonism
D) Partial agonism

Think I just drew a blank on this one, but was the answer supposed to be partial agonism? Could someone explain please?
 
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Ok I have a quick question...

60yo male comes to physician bc of 2wk history of fatigue and exercise intolerance. He was diagnosed w/stage I HTN one month ago and began treatment with propranolol. Pulse is 56/min compared to 72/min a month ago. Treatment switched to pindolol; symptoms resolve in a month and pulse is 68/min. What MoA of pindolol explains its affect on the pt's heart rate?
A) Competitive agonism
B) Competitive antagonism
C) Inverse agonism
D) Partial agonism

Think I just drew a blank on this one, but was the answer supposed to be partial agonism? Could someone explain please?

The pharm chapter in FA says that pindolol and acebutolol are partial agonists (pindolol at b1 & b2, acebutolol only at b1). That's really the only reason I got it right. Otherwise, I guess you could just reason out that pindolol had a lesser effect on b-blockade than propranolol (thus B & C are wrong), and that there would be no real reason to give a hypertensive patient an agonist (ruling out A)
 
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Can anyone help me out on the AVM question? where they showed the lady's brain with all the spongy holes in it? I'm not really sure about the pathogenesis of AVM and how it would cause a lesion like that. I tried wiki-ing it and everything, but couldn't find a good explanation. Thanks!
 

Dr McSexy

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I don't know exactly what you want to have answered. I assume you are asking why the picture looks the way it did, as opposed to the pathophysiology of AVM, which is on wiki and stuff.

I don't have access to the picture, but from what I remember it there were medium/large vessels in the lesion (maybe the spongy holes you are referring to?). It wasn't the best example(i.e. wiki has obvious large AVMs in a brain section for their picture ), but nonetheless when I looked at it, I thought it looked like most of the AVM lesions as I've seen in my path courses.
 

womp

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A 76-year-old man with congestive heart failure comes to the physician because of a 1-month history of shortness of breath after walking up a flight of stairs. He has had frequent nausea, and he has had to use two pillows to sleep during this period. Diffuse, moist crackles are heard over both lungs. There is pitting edema above the ankles. Which of the following best describes the function of the product secreted by the atrial myocytes in this patient?


A Decreased glomerular filtration rate (wrong)
B Increased sodium reabsorption
C Induction of vasoconstriction
D Inhibition of renin release (is it D?)
E Stimulation of aldosterone release

WTH, doesn't ANP vasodilate?
 

nacholibre

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Can anyone help me out on the AVM question? where they showed the lady's brain with all the spongy holes in it? I'm not really sure about the pathogenesis of AVM and how it would cause a lesion like that. I tried wiki-ing it and everything, but couldn't find a good explanation. Thanks!
The history of seizures + a cystic lesion = think Sturge-Weber. I don't know about the pathogenesis exactly but the only things that I can think of that cause cystic spaces in the brain are:
-Piloastrocytoma
-Abscess of some kind
-Lacunar stroke (it looks like it's near the internal capsule)
-AVM

it's definitely not entirely cystic so it's not Lacunar and prob not abscess
piloastrocytoma has solid and cystic spaces but the age of presentation doesn't fit that
So AVM is left
 

EaglesAllDay

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A 76-year-old man with congestive heart failure comes to the physician because of a 1-month history of shortness of breath after walking up a flight of stairs. He has had frequent nausea, and he has had to use two pillows to sleep during this period. Diffuse, moist crackles are heard over both lungs. There is pitting edema above the ankles. Which of the following best describes the function of the product secreted by the atrial myocytes in this patient?


A Decreased glomerular filtration rate (wrong)
B Increased sodium reabsorption
C Induction of vasoconstriction
D Inhibition of renin release
E Stimulation of aldosterone release

WTH, doesn't ANP vasodilate?
Edit: D...causes vasodilation of afferent and vasoconstriction of efferent...so you would have an increased gfr
 
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nacholibre

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A 76-year-old man with congestive heart failure comes to the physician because of a 1-month history of shortness of breath after walking up a flight of stairs. He has had frequent nausea, and he has had to use two pillows to sleep during this period. Diffuse, moist crackles are heard over both lungs. There is pitting edema above the ankles. Which of the following best describes the function of the product secreted by the atrial myocytes in this patient?


A Decreased glomerular filtration rate (wrong)
B Increased sodium reabsorption
C Induction of vasoconstriction
D Inhibition of renin release
E Stimulation of aldosterone release

WTH, doesn't ANP vasodilate?

ANP constricts efferent and dilates afferent - remember it's trying to get rid of water cause you are volume overloaded in CHF (so it's going to really increase your GFR "brisk diuresis." If you increase flow to the nephron then you decrease the time you have to reabsorb Na+ so the macula densa decreases it's activity = decreased RENIN.
 

Dr McSexy

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A 76-year-old man with congestive heart failure comes to the physician because of a 1-month history of shortness of breath after walking up a flight of stairs. He has had frequent nausea, and he has had to use two pillows to sleep during this period. Diffuse, moist crackles are heard over both lungs. There is pitting edema above the ankles. Which of the following best describes the function of the product secreted by the atrial myocytes in this patient?


A Decreased glomerular filtration rate (wrong)
B Increased sodium reabsorption
C Induction of vasoconstriction
D Inhibition of renin release (is it D?)
E Stimulation of aldosterone release

WTH, doesn't ANP vasodilate?

D is the right answer. ANP dilates the afferent arteriole and constricts the efferent arterioles causing an increased glomerular filtration rate.
 
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womp

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For the lithium/ADH question (administration of desmopressin with lithium)

Was the correct answer

PT: isotonic
JXT: hypotonic
Collecting duct: hypotonic

I need to be more careful reading these stems.
 

womp

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Can't believe I got the ETC carbon monoxide one wrong too.

Doesn't CO inhibit cytochrome c?

See attached.



Edit: Ah, crap... CO inhibits cytochrome c oxidase... :bang:
 

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Dr McSexy

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It inhibits Cytochrome C oxidase, which is another name for complex 4. It's made up of two heme components cytochrome a +a3, so it can also be referred to as that. The answer is E.

There was a discussion some where on this forum in a different thread, talking about this question in a little more detail I think, so you may want to check that out.

And yes, I think iso, hypo, hypo was the right answer as well.
 
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The history of seizures + a cystic lesion = think Sturge-Weber. I don't know about the pathogenesis exactly but the only things that I can think of that cause cystic spaces in the brain are:
-Piloastrocytoma
-Abscess of some kind
-Lacunar stroke (it looks like it's near the internal capsule)
-AVM

it's definitely not entirely cystic so it's not Lacunar and prob not abscess
piloastrocytoma has solid and cystic spaces but the age of presentation doesn't fit that
So AVM is left
Thanks, somehow we were NEVER exposed to AVM at school, so I never even thought about it until studying for step 1. I guess i mistook it for a really weird liquefactive necrosis lesion and picked the only ischemic thing on there (neonatal ischemic stroke).
 

womp

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Yeah me neither, never learned about AVMs.

What was the consensus on the alcoholic cerebellum question?



Gait ataxia?

Why not dysmetria or dysdiadochokinesia? Aren't those all cerebellar problems?

Where is the actual lesion?

What lobes are involved for dymetria and dysdiadochokinesia then?
 

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ijn

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Lateral cerebellum is more dysdiadochokinesia or deficits in distal limbs. Cerebellar vermis lesions give you truncal ataxia. Wernicke-Korasakoff syndrome affects the anterior cerebellar vermis, just like it affects the mamillary bodies and the ventromedial thalamic nuclei.
 

womp

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Lateral cerebellum is more dysdiadochokinesia or deficits in distal limbs. Cerebellar vermis lesions give you truncal ataxia. Wernicke-Korasakoff syndrome affects the anterior cerebellar vermis, just like it affects the mamillary bodies and the ventromedial thalamic nuclei.
Thanks!

Dude you're going to rock Step 1.
 

ipizzy

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A female newborn is delivered at 34 weeks in an advanced-care setting where special delivery systems are available. The dx of a persistent pulmonary HTN is made. Considering that the newborn can be carefully monitored for methemoglobinemia, which of the following is the most appropriate therapy?
a). Desflurane
b). Hyperbaric O2 chamber
c). Nitric oxide
d). Nitrous oxide
e). O2 diluted with He
This question was also previously discussed in the setting of the difference between nitric oxide and nitrous oxide, but why wouldn't you want to use a hyperbaric O2 chamber?
Dunno if someone already helped with this, but here's my understanding:

For newborns with pulmonary hypertension, the problem isn't ventilation (plenty of O2 gets into the alveoli just fine with each respiratory effort). The issue is poor pulmonary perfusion secondary to the pulmonary arterial hypertension.

In order to help baby breathe, you want to relieve the pulmonary hypertension. This is achieved with inhaled nitric oxide (NO), which stimulates cGMP release and vasodilation locally in the pulmonary vasculature. Dilation of the pulmonary vasculature helps more blood flow into the lungs to be oxygenated. Because it's inhaled, NO (with its short half life) doesn't make it too far into systemic circulation and won't cause problems like systemic hypotension.

I suppose hyperbaric O2 would help baby get more oxygen, but it wouldn't solve the problem of the pulmonary hypertension and baby would be stuck in the hyperbaric chamber with its right ventricle still pumping harder than it should be against all that resistance in the pulmonary vasculature
 
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Dunno if someone already helped with this, but here's my understanding:

For newborns with pulmonary hypertension, the problem isn't ventilation (plenty of O2 gets into the alveoli just fine with each respiratory effort). The issue is poor pulmonary perfusion secondary to the pulmonary arterial hypertension.

In order to help baby breathe, you want to relieve the pulmonary hypertension. This is achieved with inhaled nitric oxide (NO), which stimulates cGMP release and vasodilation locally in the pulmonary vasculature. Dilation of the pulmonary vasculature helps more blood flow into the lungs to be oxygenated. Because it's inhaled, NO (with its short half life) doesn't make it too far into systemic circulation and won't cause problems like systemic hypotension.

I suppose hyperbaric O2 would help baby get more oxygen, but it wouldn't solve the problem of the pulmonary hypertension and baby would be stuck in the hyperbaric chamber with its right ventricle still pumping harder than it should be against all that resistance in the pulmonary vasculature
I think my issue with this question was that you could easily mistake it for neonatal respiratory distress syndrome. I know they said the baby was born at 34 weeks and all, but we have no clue if mom was a poorly controlled diabetic or something. I think most people's instincts are to think "newborn with pulmonary vasoconstriction = NRDS --> give O2!" Obviously that was the wrong assumption to make here, but they could've given some sort of indication that NRDS was not the case (e.g. maybe told us that L:S > 2).

After looking it up I realized Persistent Pulmonary HTN of the Newborn is an actual condition. I don't remember the question exactly, but I don't remember them phrasing it in such a way as to indicate it's an actual condition. I think I just remember it being like "baby was diagnosed with persistent pulmonary hypertension," which seemed more like they were telling me the symptoms rather than the diagnosis. Oh well.
 

peace zealot

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Here is a question, if we have a baby with neonatal RDS, can we give hyperbaric O2? I am asking because hyperbaric O2 causes retinal neovascularization, so is there any alternative to that in neonatal RDS.
 
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EaglesAllDay

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A 26 year old woman comes to the doctors office with a 30 lb weight gain, irregular menstrual periods, constipation, and fatigue for the past 6 months. Also complains of increased difficulties with concentration and memory loss for the past month. P/e shows a bp of 145/84mmHg, dry skin and decreased musle stretch reflexes at the ankles. Serum chol is 310mg/dl and serum potassium is 4 mEq/L. Which of the following is most likely to confirm diagnosis?

A. Cortisol
B. Dehydroepiandrosterone
C. Hb A1c
D. LH
E. Prolactin
F. Testosterone
G. TSH

Can i get an explanation for this??? drawing a blank (choose cortisol and it was wrong)
 

ijn

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Here is a question, if we have a baby with neonatal RDS, can we give hyperbaric O2? I am asking because hyperbaric O2 causes retinal neovascularization, so is there any alternative to that in neonatal RDS.
High % FiO2 is used to treat these infants, not hyperbaric O2. There is no alternative beyond delaying delivery for as long as possible. Prematurity is the greatest risk factor for neovascularization, not hyperoxia. The risk of neovascularization with high FiO2 supplementation is far outweighed by the mortality associated with hypoxia.
 

ijn

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A 26 year old woman comes to the doctors office with a 30 lb weight gain, irregular menstrual periods, constipation, and fatigue for the past 6 months. Also complains of increased difficulties with concentration and memory loss for the past month. P/e shows a bp of 145/84mmHg, dry skin and decreased musle stretch reflexes at the ankles. Serum chol is 310mg/dl and serum potassium is 4 mEq/L. Which of the following is most likely to confirm diagnosis?

A. Cortisol
B. Dehydroepiandrosterone
C. Hb A1c
D. LH
E. Prolactin
F. Testosterone
G. TSH

Can i get an explanation for this??? drawing a blank (choose cortisol and it was wrong)
She likely has hypothyroidism based on her presenting symptoms. Almost every word they used to describe that patient is pretty high yield. The best test to determine thryoid function is TSH.
 

EaglesAllDay

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She likely has hypothyroidism based on her presenting symptoms. Almost every word they used to describe that patient is pretty high yield. The best test to determine thryoid function is TSH.
Lol knew i had made a complete blunder on this one. Thanks.
 

peace zealot

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Here are a few Qs, please give right answers,
1.27) 54 yr male, 2 wk history of burning epigastric pain, recently divorced, eats fast food, smokes and drinks at weekends, treated for H. pylori 1 yr back, takes 600 mg/day Ibuprofen and has epigastric tenderness. What's the greatest risk for this patient's problem?
A) High fat diet
B) Ibuprofen
C) Alcohol
D) smoking
E) recent psychosocial stressor

1.40) 38 yr female, 32 wk gestation, 2 day history of fever, nausea, vomiting, muscle aches, Temp. 102, pulse 120/min, RR 20/ min. Picture of Gm stain was given. What's the organism?
A) Gardnerella
B) Corynaebac urealyticum
C) Listeria
D) Rhodococcus
E) Staph. aureus

4.41) Pt. with metastatic colon ca has maintained remission by taking Bevacizumab as a single agent. The ability to administer this agent despite it being a foreign protein is a result of which?
The agent is:
A) Humanized Ab
B) Variable region of murine Ab directed against VEDGF
C) B cell dysfunction
D) Immune suppression because of previous chemotherapy
E) T cell dysfunction

Patient has Mitochondrial hereditary disease. I think the answer was Defect in Oxidative phosphorylation, I put Defect is B oxid. of Fatty acids. can someone explain why?
 

ijn

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1.27 Of that list NSAIDS are the most associated ulcers; smoking increases your risk by 50%.

1.40 I was never 100% sure on this one. She appears to have some sort of systemic infection, maybe meningitis. The picture is crap in my opinion. I think they're showing gram positive coccobacilli, so the answer would be Listeria monocytogenes. Pregnancy is a risk factor and major buzz word for that infection.

4.41 it's a humanized monoclonal antibody - meaning we recognize the Fc region as self. If it was horse Fc or something, like some antivenoms, then we could end up in anaphylaxis upon repeat administration.

I don't know why it wouldn't be beta oxidation. Maybe those proteins are made by host genomes rather than mitochondrial genome. Or maybe most documented mitochondrial defects are associated with oxidative phosphorylation.
 

womp

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1.40 I was never 100% sure on this one. She appears to have some sort of systemic infection, maybe meningitis. The picture is crap in my opinion. I think they're showing gram positive coccobacilli, so the answer would be Listeria monocytogenes. Pregnancy is a risk factor and major buzz word for that infection.
She also had fever I think. Listeria is only gram positive bacteria with endotoxin. At least that was my rationale.
 

ipizzy

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Patient has Mitochondrial hereditary disease. I think the answer was Defect in Oxidative phosphorylation, I put Defect is B oxid. of Fatty acids. can someone explain why?
I chose oxidative phosphorylation because the question stem mentioned the patient had increased serum lactate levels (implying problems with carrying out the TCA cycle and thus less substrate for oxidative phosphorylation is being produced). I don't know why beta oxidation is incorrect though, I just thought oxidative phosphorylation fit better with the info given in the question :shrug:
 

hotchik

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A 40-year-old man comes to the physician because of a 6-month history of difficulty maintaining an erection during sexual intercourse. He has consumed 1/2 L of bourbon daily for 15 years. His pulse is 88/min, and blood pressure is 130/80 Hg. Examination shows scleral icterus and spider angiomata over the trunk. The liver span is 5 to 6 cm in the midclavicular line. The spleen tip is palpated 5 to 6 cm below the left costal margin. Decreased serum concentrations of which of the following is the most likely cause of this patient's erectile dysfunction?

A) Estradiol
B) Estrone
C) FSH
D) HCG
E) LH
F) testosterone

Wouldn't we get decreased serum LH due to hyperestrogenisms --> decreased testosterone in the testes? plz elaborate with mechnism thanks in advanced!

Btw, E is incorrect
 

Lonely Sol

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I thinkits because decrease in LH is not the primary cause of erectile dysfunction, but decrease in testosterone is.

Sorry..but i dont know the mechanism for it
 

Ok2Panic

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A 40-year-old man comes to the physician because of a 6-month history of difficulty maintaining an erection during sexual intercourse. He has consumed 1/2 L of bourbon daily for 15 years. His pulse is 88/min, and blood pressure is 130/80 Hg. Examination shows scleral icterus and spider angiomata over the trunk. The liver span is 5 to 6 cm in the midclavicular line. The spleen tip is palpated 5 to 6 cm below the left costal margin. Decreased serum concentrations of which of the following is the most likely cause of this patient's erectile dysfunction?

A) Estradiol
B) Estrone
C) FSH
D) HCG
E) LH
F) testosterone

Wouldn't we get decreased serum LH due to hyperestrogenisms --> decreased testosterone in the testes? plz elaborate with mechnism thanks in advanced!

Btw, E is incorrect
F I think
I think it's because increased conversion of testosterone to estrogen. that's how you get the spider angioma, small testicles and gynecomastia in chronic alcoholism too iirc
 

hotchik

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F I think
I think it's because increased conversion of testosterone to estrogen. that's how you get the spider angioma, small testicles and gynecomastia in chronic alcoholism too iirc
thanks all for the reply...i found in one of my notes that a probable mechanism is due to hyperestrogenism --> increased SHBG (remember estrogen increases SHBG and TBG) --> decreased free testosterone --> leading to sexual dysfunction
 

spyderracing32

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Ultrasound won't reliably pick up the fetus until week . . . well I don't know but way later than hCG. I want to say week 7 or 8.

I hate to perseverate or derail the thread, but doesn't anyone who got right answer remember the question I posted on the last page? The elderly woman with the long chronic condition who dies in the hospital and they show a gross picture of her spine.
It's also way cheaper to pee on an indicator than fire up the ol' U/S. Cheap and reliable is always the right answer.
 

spyderracing32

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I chose oxidative phosphorylation because the question stem mentioned the patient had increased serum lactate levels (implying problems with carrying out the TCA cycle and thus less substrate for oxidative phosphorylation is being produced). I don't know why beta oxidation is incorrect though, I just thought oxidative phosphorylation fit better with the info given in the question :shrug:
Because a deficiency in the enzymes responsible for beta oxidation wouldn't cause lactic acidosis since you're still able to regenerate NAD+ from NADH through oxidative phosphorylation. The giveaway for someone who has beta-oxidation problems would be someone who is hypoketonemic with starvation because you need to make Acetyl-CoA to make ketones.
 

peace zealot

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A 40-year-old man comes to the physician because of a 6-month history of difficulty maintaining an erection during sexual intercourse. He has consumed 1/2 L of bourbon daily for 15 years. His pulse is 88/min, and blood pressure is 130/80 Hg. Examination shows scleral icterus and spider angiomata over the trunk. The liver span is 5 to 6 cm in the midclavicular line. The spleen tip is palpated 5 to 6 cm below the left costal margin. Decreased serum concentrations of which of the following is the most likely cause of this patient's erectile dysfunction?

A) Estradiol
B) Estrone
C) FSH
D) HCG
E) LH
F) testosterone

Wouldn't we get decreased serum LH due to hyperestrogenisms --> decreased testosterone in the testes? plz elaborate with mechnism thanks in advanced!

Btw, E is incorrect
The answer is decreased level of testosterone, because in hepatic cirrhosis there is decreased degradation of estrogen and 17-ketosteroids and also there is increased conversion of testosterone into estrogen in adipose tissue.
 
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This thread is lovely, thank you.

I have a few more questions.

The CREST syndrome question involving esophageal motility. Was the answer decreased LES and peristalsis? I was thinking CREST and achalasia were friends so I had the LES tone arrow up.

Can anyone further explain why the answer to this was "homing": The question about mice melanoma that spreads everywhere, until you inject an antibody in the liver that protects the liver from the mets. I went with invasion. Fail.

There was the young girl who clearly had albinism-like characteristics, neutropenia, but recurrent bacterial infections. I went with decreased NADPH oxidase but that was incorrect. I must be missing some association on this one...

Kid with either Becker/Duchenne had weak adduction, and weakness of an additional muscle that attaches where? Answer was previously listed as ischium. But I am terrible at anatomy from having a hardcore orthopod prodigy attack my cadaver (and not paying attention, clearly). Which muscle are they talking about? Thanks. I am terrible at anatomy.

Gentamicin/aminoglycoside toxicity at the tubules. I went with collecting tubule. Was proximal correct?

Doctor was trying to give a drug for cough suppression that would not cause constipation or addiction. I ended up going with tramodol because all of the others seemed addicting. Anyone know the correct answer for this one?

Trucker sitting in car for 10 hours goes through with a V/Q scan. I am assuming he had a PE. I went with Decreased ventilation with normal perfusion. This was wrong.

Any help would be great. I apologize for not posting the answer choices. UWorld has me conditioned not to try and print screen or copy anything.

Also, has anyone that has taken Step 1 have any advice on the most predictive test? I was scoring 240s on UWorld Assessments, the 150Q free practice test, and DIT's end of course exam. But my NBME scores these last couple days have been 230ish. Not a good sign close to exam day.

Thanks and good luck to all.
 
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