USMLE NBME 18 - Questions and Answers - Discussions & Explanations

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TheAberrantGene

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NBME 18 has been released and is available on regular and extended feedback.
I will be taking it fairly soon as my exam is around the corner.
Let's continue the great trend on this forum and start a discussion once people start taking it,

Best of luck fellas ! :)

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12 hours after aspirin suicide attempt. tachypnea. lab findings?
pH, Pco2, HCO3 ?

You'll have metabolic acidosis. pH will be low (below 7.35), bicarb will be low (below 24), and pCO2 will be low (below 40) as patient hyperventilates trying to compensate for the metabolic acidosis. Also of note, this metabolic acidosis will have an increased anion gap, as salicylic acid will nudge down the normal anions (Cl- and bicarb) a bit.
 
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You'll have metabolic acidosis. pH will be low (below 7.35), bicarb will be low (below 24), and pCO2 will be low (below 40) as patient hyperventilates trying to compensate for the metabolic acidosis. Also of note, this metabolic acidosis will have an increased anion gap, as salicylic acid will nudge down the normal anions (Cl- and bicarb) a bit.
True. And the PCO2 will be actually lower than what is predicted by the winter's formula(PCO2 = 1.5 × [HCO3-]) + 8 ± 2) because of the superimposed respiratory alkalosis.
 
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There was a pdf or something made by someone which was doing the rounds. It had all the explanations and answers to the NBME 18.
Anybody got it ?
 
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a 35 year old women comes to the physician bcz of fever n sharp chest pain for 3 days. temp= 101.3. friction rub heard. al the secondary causes of pericarditis is ruled out. most likely cause of primary pericarditis?
A. bacterium
B. fungus
c. parasite
d. tumor
e. virus


Yeah it's E somewhere I saw mcc of peri/myocarditis is viral (coxsackie B like @chillaxbro said)
 
Can someone tell me the answer to this one?

View attachment 201777

Ileocolic --> superior mesenteric --> portal --> right hepatic branch of portal

A 21-year old woman comes to the physician because of 10-day history of difficulty walking. Two years ago, she had loss of vision int he left eye which improved over 2 months. Neurologic examination shows decreased visual acuity in the left eye with pallor of optic disc. She has past-pointing on a finger-nose test. She has a broad-based gait. An MRI of the brain shows lesion in the white matter of cerebellum. Which of the following describes the pathogenesis of the disease process in this patient?

A. Antibodies with specificity to axonal microtubules bind to surface of axons
B. CD4+ T lymphocytes are activated by myelin basic protein
C. CD8+ T lymphocytes kill astrocytes
D. Complexes of rheumatoid factor and IgG are deposited in choroid plexus
E. Inflammatory vasculitis affects perforating arterioles

A. CD4+ T lymphocytes are activated by myelin basic protein


a 35 year old women comes to the physician bcz of fever n sharp chest pain for 3 days. temp= 101.3. friction rub heard. al the secondary causes of pericarditis is ruled out. most likely cause of primary pericarditis?
A. bacterium
B. fungus
c. parasite
d. tumor
e. virus

E. Virus
 
There was a pdf or something made by someone which was doing the rounds. It had all the explanations and answers to the NBME 18.
Anybody got it ?

Power of Google. I just searched testpirates NBME 18

I didn't see explanations, but all the answers for anyone who wants to check the ones that haven't been answered here.
 
Hi all, my test date is getting pretty close and I may just be losing my mind but I have a question regarding the tennis player's renal status. I saw where the question was answered already on here but have a question as to why. So to backup for a second, we have a dehydrated player and we want to know hyper/iso/hypotonic status of prox tubule/ macula densa/ collecting tubules. So, now really backing up here, when fluid is filtered into bowman's capsule- it is isotonic to the rest of the plasma, correct? But the prox tubule's main job is to reabsorb like crazyyy and, therefore, I went with hypotonic for the PT's status (bc it was losing na/bicarb/etc so now has a ton less 'stuff' in it than regular plasma). Why is this wrong? Is it because water is reabsorbed from the PT at an equal rate and this is, in fact, what 'isotonic' is referring to? Thanks a million!!!
 
Hi all, my test date is getting pretty close and I may just be losing my mind but I have a question regarding the tennis player's renal status. I saw where the question was answered already on here but have a question as to why. So to backup for a second, we have a dehydrated player and we want to know hyper/iso/hypotonic status of prox tubule/ macula densa/ collecting tubules. So, now really backing up here, when fluid is filtered into bowman's capsule- it is isotonic to the rest of the plasma, correct? But the prox tubule's main job is to reabsorb like crazyyy and, therefore, I went with hypotonic for the PT's status (bc it was losing na/bicarb/etc so now has a ton less 'stuff' in it than regular plasma). Why is this wrong? Is it because water is reabsorbed from the PT at an equal rate and this is, in fact, what 'isotonic' is referring to? Thanks a million!!!
Exactly. Water follows whatever you reabsorb in the PCT because it is permeable to water. In the ascending tubule, water is not permeable so when you absorb solutes it becomes hypotonic
 
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Couldnt find explanation for this :


48 yo woman with gradual onset of pain for 2 wks .No H/o trauma ,smoking , alcohol or drugs .Hemogram , serum studies and urinalysis are normal .Spine x ray shows lytic lesions at T10 and L1 .dx ?
1) avascular necrosis
2) metastatic ca of breast >>> is this the answer?
3) osteosarcoma
4) renal osteodystropy
5) thyroid ca

how does osteosarcoma look ? sunburst etc but it should still be lytic .Should breast ca have some correlation with alcohol and smoking ?
 
Can someone explain this to me please .The more I read neuro the more mistake I make it seems .
Screenshot 2016-04-03 11.44.45.png




Q2 :Where can I read the details of the toxins for strep pyogenes and what they do ? I was able to choose erythrogenic toxin on the basis of exclusion .
 
Can someone explain this to me please .The more I read neuro the more mistake I make it seems .View attachment 202032



Q2 :Where can I read the details of the toxins for strep pyogenes and what they do ? I was able to choose erythrogenic toxin on the basis of exclusion .

1. It's describing Guillain Barré.. could only be myelinated fibers that it's affecting in this vignette. (Ascending bilateral weakness/numbess)

2. Streptococcal toxic shock syndrome! I learned that toxin in class but I believe it's also in first aid. All of the important toxins are definitely listed in first aid. It may go by a different name but think about what is happening in toxic shock.
 
Couldnt find explanation for this :


48 yo woman with gradual onset of pain for 2 wks .No H/o trauma ,smoking , alcohol or drugs .Hemogram , serum studies and urinalysis are normal .Spine x ray shows lytic lesions at T10 and L1 .dx ?
1) avascular necrosis
2) metastatic ca of breast >>> is this the answer?
3) osteosarcoma
4) renal osteodystropy
5) thyroid ca

how does osteosarcoma look ? sunburst etc but it should still be lytic .Should breast ca have some correlation with alcohol and smoking ?

Metastatic breast cancer ---->>> lytic lesions in T10 and L1. One of the most common mets from breast cancer is to the bone. Same for prostatic cancer. Always gotta remember the most commons...it helps a ton and pulls you away from thinking too much into it.

My path professor for musculoskeletal was amazing. He always said whenever you have a 16 year old with pain in the knee it's always osteosarcoma which is why this isn't the answer here. So, that is what I always think of. For this question though, you gotta go back to the most common.
 
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1. It's describing Guillain Barré.. could only be myelinated fibers that it's affecting in this vignette. (Ascending bilateral weakness/numbess)

2. Streptococcal toxic shock syndrome! I learned that toxin in class but I believe it's also in first aid. All of the important toxins are definitely listed in first aid. It may go by a different name but think about what is happening in toxic shock.


Are you sure about GB syndrome ; its predominantly motor and involves proximal muscles first ; no H/o enteritis , pneumonia or viral infection .The question focusses on the cause of sensory findings ; considering pt has ataxia how can we differentiate from spinocerebellar tract lesions ?:help:
 
A 35 YO woman brought to emergency, passed out. Husband tells the physician that the patient has bulimia nervosa which laboratory test results indicating recurrent vomiting ?
Potassium, Bicarbonate, Anion Gap, pH
a. Decrease, Increase, Normal, Increase
b. Increase, Decrease Normal, Increase
 
A 35 YO woman brought to emergency, passed out. Husband tells the physician that the patient has bulimia nervosa which laboratory test results indicating recurrent vomiting ? Pt will be in metabolic alkalosis because she is losing stomach acid to vomitting : K decrease , HCo3 increase , anion gap normal , PH increase
Potassium, Bicarbonate, Anion Gap, pH
a. Decrease, Increase, Normal, Increase
b. Increase, Decrease Normal, Increase
 
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Are you sure about GB syndrome ; its predominantly motor and involves proximal muscles first ; no H/o enteritis , pneumonia or viral infection .The question focusses on the cause of sensory findings ; considering pt has ataxia how can we differentiate from spinocerebellar tract lesions ?:help:

I went straight for GBS and myelinated fibers because of the ascending bilateral numbness. As far as I know, sensory findings can be present before the motor weakness. As far as the ataxia goes... there's a rare "Fisher variant" that the patient can present with ataxia as well. One thing I learned while doing UWorld and these NBMEs is not to think too much into it. My gut on this said GBS because of what I said above and helped me to the right answer.

Anyone else feel free to give input...

http://www.score95.com/blog/blog/usmle-guillain-barre-syndrome/
 
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What is the dx here .What is the correlation with c jun , Myosin heavy chain and endothelin ?



Screenshot 2016-04-03 14.31.44.png
 
Q- 30 year old woman with a long history of PID has a surgical resection of a scarred segment of a fallopian tube which of the foll inflammatory cells are most likely to be found ?
eosinophils
neutrophils
macrophages >>>> is this the answer only because this is a CHRONIC infection ?
mast cells
basophils


How to approach this question ?
Screenshot 2016-04-03 14.41.36.png


Q3 ) 29 year old has PCOS .Pt advises her to lose weight .Is the answer : provide follow up appointments to assess progress in attaining her goals ?
 
I went straight for GBS and myelinated fibers because of the ascending bilateral numbness. As far as I know, sensory findings can be present before the motor weakness. As far as the ataxia goes... there's a rare "Fisher variant" that the patient can present with ataxia as well. One thing I learned while doing UWorld and these NBMEs is not to think too much into it. My gut on this said GBS because of what I said above and helped me to the right answer.

Anyone else feel free to give input...

http://www.score95.com/blog/blog/usmle-guillain-barre-syndrome/

One thing I forgot to mention here @zeevee is also if you have decreased proprioception...you definitely don't know where you're stepping = ataxia.
 
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Q- 30 year old woman with a long history of PID has a surgical resection of a scarred segment of a fallopian tube which of the foll inflammatory cells are most likely to be found ?
eosinophils
neutrophils
macrophages >>>> is this the answer only because this is a CHRONIC infection ?
mast cells
basophils


How to approach this question ?
View attachment 202041

Q3 ) 29 year old has PCOS .Pt advises her to lose weight .Is the answer : provide follow up appointments to assess progress in attaining her goals ?

Yes, because it is chronic... scarring = macrophages.

Next one is somewhere as well in this thread I can't remember the explanation...I got that one wrong, ha.

3rd one yes, you want to increase the likelihood of her adherence so by following up and monitoring her progress she would be more likely to be successful (with support of physician.)
 
Go back in this thread, this one is discussed somewhere.

This is the explanation someone has on page 4 :

The question had to do with ventricular hypertrophy if I'm not mistaken. So B-myosin heavy chain would increase. This leads to a diastolic dysfunction in which the ventricle can't accommodate all the blood and so there's backup. Eventually this is gonna lead to pulmonary HTN which is where endothelium comes into play. (I base this on the fact that the drug Bosentan is used in pulm HTN and antagonizes endothelin). So endothelin will increase. In order for this process to progress, C-JUN needs to increase because it is anti-apoptotic... This was my logic in doing this question (except when I did it I had to guess on C-JUN)."

seems like the person is just talking to himself .
 
This is the explanation someone has on page 4 :

The question had to do with ventricular hypertrophy if I'm not mistaken. So B-myosin heavy chain would increase. This leads to a diastolic dysfunction in which the ventricle can't accommodate all the blood and so there's backup. Eventually this is gonna lead to pulmonary HTN which is where endothelium comes into play. (I base this on the fact that the drug Bosentan is used in pulm HTN and antagonizes endothelin). So endothelin will increase. In order for this process to progress, C-JUN needs to increase because it is anti-apoptotic... This was my logic in doing this question (except when I did it I had to guess on C-JUN)."

seems like the person is just talking to himself .
Well... the logic is there though. I don't think we ever really came up with the exact reasoning behind c-jun other than it's a transcription factor so it'd have to increase.
 
Can someone explain these questions?

1) 3-year-old boy with progressive fever and skin lesions during 24 hours. T 102.9 F, pulse 120, RR 20, bp 110/60. PE shows large, flaccid, bullous lesions over trunk and abdomen. Another finding in patient?

---Why is it positive nares culture for toxin-producing staph aureus?


2) Full-term newborn in respiratory distress. Imaging shows abdominal contents in left pleural cavity. Maldevelopment of which structure led to diaphragm defect?

--Esophageal mesoderm
--Left diaphragmatic crus (picked this one. WRONG)
--Left pleuropericardial fold
--Left pleuroperitoneal membrane
--septum transversum

3) 20-year-old woman with palpable lump in right breast 4 months, no pain, swelling or nipple discharge. Lump is smooth, firm, round, mobile, nontender, well delineated. No skin change. Dx?

Why is it fibroadenoma and not cyst?
 
Can someone explain these questions?

1) 3-year-old boy with progressive fever and skin lesions during 24 hours. T 102.9 F, pulse 120, RR 20, bp 110/60. PE shows large, flaccid, bullous lesions over trunk and abdomen. Another finding in patient?

---Why is it positive nares culture for toxin-producing staph aureus






2) Full-term newborn in respiratory distress. Imaging shows abdominal contents in left pleural cavity. Maldevelopment of which structure led to diaphragm defect?

--Esophageal mesoderm
--Left diaphragmatic crus (picked this one. WRONG)
--Left pleuropericardial fold
--Left pleuroperitoneal membrane
--septum transversum

3) 20-year-old woman with palpable lump in right breast 4 months, no pain, swelling or nipple discharge. Lump is smooth, firm, round, mobile, nontender, well delineated. No skin change. Dx?

Why is it fibroadenoma and not cyst?

1. Toxic shock syndrome. Almost everyone has staph aureus colonized in their nares and it's the only one that fits in this case since they have desquamation of their skin and fever.

2. Gastric contents where lungs are ---> pulmonary hypoplasia ----> respiratory distress = failure of pleuroperitoneal membrane to fuse.

3. Age of patient + lump is smooth, firm, round, mobile, nontender...most common breast tumor for this age group and this description is a fibroadenoma. Textbook definition. Cystic would be > 25, premenstrual pain, multiple, and usually bilateral.
 
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section 3, 29/50:
Healthy 5yo boy comes for motion sickness. Parents want to give dyphenhydramine before a trip. Whats the mecanism of action of the drug - for motion sickness :
a) agonist alpha1 adrenoreceptors
b) agonist beta1 adrenoreceptors
c)agonist N-methyl-D-aspartate receptors
d)antagonist histamine 2 receptors (I know its H1, but thats the closest I figure out - wrong)
e) antagonist M3 receptors (is this one?)
f) antaagonist serotonin receptors

Thanks a lot!
yes its E, antagonist M3 receptors

This question really tripped me up. I thought diphenhydramine's primary action is as an H1 antagonist (H1 blockers can cross the BBB, where they have an antiemetic effect on the H1 receptors in the NTS...?)

I guess I probably should have picked antimuscarinic anyway, but the M3 part tricked me too because I thought the M1 receptors are the ones in the CNS. I think I ended up saying 5-HT antagonist activity because it was the only one I reasoned would have an antiemetic CNS effect. Did I just way overthink this one?
 
Can someone help with these?

11. 39-year-old man with 1-week of red spots on shins, joint pain and fatigue. PE shows purpura over lower extremities. Liver palpated 4 cm below costal margin. Labs: WBC 10,000, AST 142, ALT 154, hepatitis C virus RNA positive, anti-hepatitis C virus antibody positive, cryoglobulins positive, C4 120 (N=350-600), urine protein 4+, urine RBC numerous. Hypersensitivity reaction?
- Type III (immune complex-mediated)


26. 50-year-old woman with COPD comes with 3 months of progressive shortness of breath. Physical shows JVD, loud pulmonary component of S2. Pulmonary function tests show FEV1:FVC ratio of 20% and decreased diffusing capacity for carbon monoxide. Which is decreased in pulmonary vascular smooth muscle?
- Endothelial nitric oxide synthase production

39. 50-year-old man with pulmonary embolus. Treated with intravenous heparin. 24 hours later, warfarin added. Day 2, partial thromboplastin time is 52 seconds (control 26 sec), and prothrombin time is 12 seconds (control 12.1 sec; INR = 1). Best explanation for normal prothrombin time and INR?
- Long half-life of factor II (prothrombin) (?)

33. Researching new cancer drug, effective at killing rapidly dividing cells, in mice caused profound myelosuppression. In patients, most appropriate to follow which when at risk for infectious complications?
- Neutrophil counts

26. 64-year-old with non-Hodgkin lymphoma and 3-day history of abdominal pain and nausea. T 99.7F, HR 100, bp 130/80. Abdominal exam tenderness of flanks and lower quadrants. BUN 34 and creatinine 3.8. CT shows bilateral hydronephrosis and lymphadenopathy compressing ureters. Tx to improve renal function?
- Bilateral stents in the ureters


Thank you!
 
Hey y'all- I scored a scaled 245 on form 18 and it was my last self assessment before the real deal.

Just got my actual step 1 score today and got a 248. Id say this was a pretty accurate assessment.
 
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This question really tripped me up. I thought diphenhydramine's primary action is as an H1 antagonist (H1 blockers can cross the BBB, where they have an antiemetic effect on the H1 receptors in the NTS...?)

I guess I probably should have picked antimuscarinic anyway, but the M3 part tricked me too because I thought the M1 receptors are the ones in the CNS. I think I ended up saying 5-HT antagonist activity because it was the only one I reasoned would have an antiemetic CNS effect. Did I just way overthink this one?

I don't think you should just say H2 receptors are close enough to H1 and just choose it. Remember those 2 are very different (H2, Gs, part of parietal cells secreting acid function) while H1 receptors are in smooth muscle (Gq) and have to do with your usual OTC antihistamines and what not.
 
Can someone help with these?

11. 39-year-old man with 1-week of red spots on shins, joint pain and fatigue. PE shows purpura over lower extremities. Liver palpated 4 cm below costal margin. Labs: WBC 10,000, AST 142, ALT 154, hepatitis C virus RNA positive, anti-hepatitis C virus antibody positive, cryoglobulins positive, C4 120 (N=350-600), urine protein 4+, urine RBC numerous. Hypersensitivity reaction?
- Type III (immune complex-mediated)
Sounds like Henoch-Schnolein purpura to me. They just left out the word "palpable" to make it more difficult. HSP causes Ag/Ab complexes that deposit in tissues so Type III.


26. 50-year-old woman with COPD comes with 3 months of progressive shortness of breath. Physical shows JVD, loud pulmonary component of S2. Pulmonary function tests show FEV1:FVC ratio of 20% and decreased diffusing capacity for carbon monoxide. Which is decreased in pulmonary vascular smooth muscle?
- Endothelial nitric oxide synthase production

Hypoxic vasoconstriction is a unique feature of the lung where it shunts blood away from areas with poor ventilation to go for the "good alveoli" instead of vasodilating vessels to increase flow (as seen in other organs during an ischemic event). So NO synthesis will decrease.

39. 50-year-old man with pulmonary embolus. Treated with intravenous heparin. 24 hours later, warfarin added. Day 2, partial thromboplastin time is 52 seconds (control 26 sec), and prothrombin time is 12 seconds (control 12.1 sec; INR = 1). Best explanation for normal prothrombin time and INR?
- Long half-life of factor II (prothrombin) (?)

When you start a patient on anticoagulants like Warfarin, you usually start Heparin too to avoid the hypercoagulable state induced by warfarin (Warfarin knocks out protein C & S as well, and protein C's half life is only 14 hours, longer than most of the other coag factors (except Factor VII), so you gotta give heparin to avoid this hypercoagulable state). Heparins effect is on ATIII which is endogenously present in our vessels so its effect is immediate, shown as the elevated PTT. But the PT/INR is still normal because the half life of PT (Factor II) is 60 hours, longest of them all so it takes time to actually increase the PT.

33. Researching new cancer drug, effective at killing rapidly dividing cells, in mice caused profound myelosuppression. In patients, most appropriate to follow which when at risk for infectious complications?
- Neutrophil counts

When we talk about drugs that cause bone marrow suppression (Clozapine, Carbamazepine, PTU/Methimazole, Colchicine), we're mostly worried about neutropenia, leading to infections.

26. 64-year-old with non-Hodgkin lymphoma and 3-day history of abdominal pain and nausea. T 99.7F, HR 100, bp 130/80. Abdominal exam tenderness of flanks and lower quadrants. BUN 34 and creatinine 3.8. CT shows bilateral hydronephrosis and lymphadenopathy compressing ureters. Tx to improve renal function?
- Bilateral stents in the ureters

I got this right, but I wasn't too sure about it when I was choosing that answer. I figured why not just do something about the LAD, but it wasn't a choice, lol. So I figured the stents would be the next best option.


Thank you!

Answers in bold
 
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1) A 63 year old man comes to the physician b/c of abnormal BP reading taken during a health fair. No PMHx of major medical illness. 6 months ago his BP was 135/85, today it's 170/98, a bruit is heard over the left renal artery. Spiral CT angiography shows left arterial stenosis. Which of the following sets of changes is most likely in this patient?

TPR Plasma renin activity Serum aldosterone concentration
I chose decrease increase increase.
I basically started with the increase in renin activity which is obviously d/t decreased renal perfusion, which would increase aldo. So I was left with either TPR goes up or down. I maybe overthought it, but I thought, increased aldo leads to increased BV, so increased Q and increased BP through the carotid baroreceptors leads to increased firing thru the baroreceptors, and compensatory decreased sympathetic output leads to vasodilation and decreased TPR. Was this wrong?

2) A 63 year old woman comes to the physician b/c of a 2 week history of daily episodes of severe, lancinating, left-sided facial pain. The pain, which occurs suddenly and lasts 30 to 60 seconds, shoots from the left ear down along the jawline. The pain is sometimes precipitated by chewing or brushing teeth. Vital signs are normal. PE shows no abnormalities except for moderate dental caries . Diagnosis?

A- Cluster headache
B- Dental abscess
C- Temporal arteritis
D- Temporal lobe epilepsy
E- Temporomanidbular joint syndrome (wrong)
F- Trigeminal neuralgia

2) A 45 year old homeless man is brought to the emergency dept by police 30 min after he was found unconscious. His breath and clothes smell of alcohol. T 36.8 C (98.2 F), pulse 68, RR 14, BP 110/55, PE shows bronzed skin and spider angiomata on the chest. Lab studies show:

Hb: 10
Hct: 30%
MCV: 110
Leuks: 9000
Segmented neutros 70%
Lymphocytes 20%
Monocytes 10%
Plt ct 160,000
Serum Ferritin 200
Serum Vit B12 500 (within normal limits)
RBC folate 20 (low. Normal 166-640)

A peripheral blood smear shows occasional hypersegmented neutrophils and 3+ oval macrocytes. Serum studies most likely to show which of the following sets of additional findings?

Methylmalonic acid Homocysteine
Various choices of increased or decrease, or normal. I chose normal and normal, which was wrong. I immediatly eliminated all the choices showing a chance in MMA as that would indicate B12 def, but wasn't sure about homocysteine. I figured since there's no B12 or B6 deficiency, the enzymes Homocysteine methyltransferase (Methionine synthetase) and Cystathione B-synthetase should both be working fine, so there should be no change in homocysteine levels. But I was wrong.

3) The question about the 70 year old woman on PE shows the anterior vaginal wall protruding downward during Valsalva, why is this not uterine prolapse? I actually didn't know what a cystocele even was until reading the above explanations for the answer, but I remember during my ward rounds in school seeing a patient with a uterine prolapse. It basically looked the same as the description in the question. She was an old lady too.

Thank you!
 
Last edited:
1) A 63 year old man comes to the physician b/c of abnormal BP reading taken during a health fair. No PMHx of major medical illness. 6 months ago his BP was 135/85, today it's 170/98, a bruit is heard over the left renal artery. Spiral CT angiography shows left arterial stenosis. Which of the following sets of changes is most likely in this patient?

TPR Plasma renin activity Serum aldosterone concentration
I chose decrease increase increase.
I basically started with the increase in renin activity which is obviously d/t decreased renal perfusion, which would increase aldo. So I was left with either TPR goes up or down. I maybe overthought it, but I thought, increased aldo leads to increased BV, so increased Q and increased BP through the carotid baroreceptors leads to increased firing thru the baroreceptors, and compensatory decreased sympathetic output leads to vasodilation and decreased TPR. Was this wrong?

2) A 63 year old woman comes to the physician b/c of a 2 week history of daily episodes of severe, lancinating, left-sided facial pain. The pain, which occurs suddenly and lasts 30 to 60 seconds, shoots from the left ear down along the jawline. The pain is sometimes precipitated by chewing or brushing teeth. Vital signs are normal. PE shows no abnormalities except for moderate dental caries . Diagnosis?

A- Cluster headache
B- Dental abscess
C- Temporal arteritis
D- Temporal lobe epilepsy
E- Temporomanidbular joint syndrome (wrong)
F- Trigeminal neuralgia

2) A 45 year old homeless man is brought to the emergency dept by police 30 min after he was found unconscious. His breath and clothes smell of alcohol. T 36.8 C (98.2 F), pulse 68, RR 14, BP 110/55, PE shows bronzed skin and spider angiomata on the chest. Lab studies show:

Hb: 10
Hct: 30%
MCV: 110
Leuks: 9000
Segmented neutros 70%
Lymphocytes 20%
Monocytes 10%
Plt ct 160,000
Serum Ferritin 200
Serum Vit B12 500 (within normal limits)
RBC folate 20 (low. Normal 166-640)

A peripheral blood smear shows occasional hypersegmented neutrophils and 3+ oval macrocytes. Serum studies most likely to show which of the following sets of additional findings?

Methylmalonic acid Homocysteine
Various choices of increased or decrease, or normal. I chose normal and normal, which was wrong. I immediatly eliminated all the choices showing a chance in MMA as that would indicate B12 def, but wasn't sure about homocysteine. I figured since there's no B12 or B6 deficiency, the enzymes Homocysteine methyltransferase (Methionine synthetase) and Cystathione B-synthetase should both be working fine, so there should be no change in homocysteine levels. But I was wrong.

3) The question about the 70 year old woman on PE shows the anterior vaginal wall protruding downward during Valsalva, why is this not uterine prolapse? I actually didn't know what a cystocele even was until reading the above explanations for the answer, but I remember during my ward rounds in school seeing a patient with a uterine prolapse. It basically looked the same as the description in the question. She was an old lady too.
_________________________________________________
First one everything increases. More renin = vasoconstriction.

The facial pain question is a pretty textbook description of trigeminal neuralgia.

Homeless guy is folate deficient so he'll have an elevated homocysteine. Take a peek at the pathway- it requires folate.

Fourth one isn't prolapse because that prolapse would cause the uterus to squish out of the vagina. Instead, you feel a bulge on the anterior wall of the vagina with increased abdominal pressure. The bladder is anterior to the uterine wall, so there's your answer.
 
Whats the overall opinion of this NBME..
many say its within +/- 1/2 points of the real deal in terms of accuracy of predictability.. what do you lot think ?
 
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Do you guys know if there is a different curve for each NBME? I just took 17 and 18, didn't pay for the extended version but reviewed answer keys online, and I got a 670 --> 264 on both of them - yet I believe I got 9 questions wrong on NBME 17 but 12 wrong on NBME 18.
 
Do you guys know if there is a different curve for each NBME? I just took 17 and 18, didn't pay for the extended version but reviewed answer keys online, and I got a 670 --> 264 on both of them - yet I believe I got 9 questions wrong on NBME 17 but 12 wrong on NBME 18.

You are correct
 
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245 on form 18, 248 on real deal.

I hope this works for me. Took UWSA1 and NBME 18 on Monday and my exam is tomorrow. Did significantly better on these from others simply because I didn't go back and change answers and got my nervousness under control. Insert eye roll here.
 
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I really want to believe what everyone is saying about this NBME being representative of the real deal, but my practice exam scores have only gone down since I took this one...my raw score was something like 600 on this (2 weeks ago), 570 on nbme 16 (one week ago) and predicted 238 on UWSA2 a few days ago. Maybe I just had a bunch of lucky guesses.
 
Hi everyone,

Can someone please explain the following:

68 year old with 10 month history of SOB and welling of his feet. FHx of CV disease, smoked 2 packs of cigarettes daily for 50 years. Pulse is 80/min, respirations are 24/min, and BP is 150/80 mmHg. PE shows 3+ pitting edema on LE, diffuse and scattered wheezes are heard bilaterally. Cardiac exam shows grade 2/6 pansystolic murmur heard best at the lower LSB, which increases on inspiration. The PMR is palpated in the sub-xiphoid area. S1 and S2 sound distant. Ab Exam shows a liver span of 14 cm. Which of the following is the likely dx?
A) Aortic stenosis
B) Cardiac amyloidosis
C) Cor pulmonale
D) CAD
E) primary pulm HTN
 
Hi everyone,

Can someone please explain the following:

68 year old with 10 month history of SOB and welling of his feet. FHx of CV disease, smoked 2 packs of cigarettes daily for 50 years. Pulse is 80/min, respirations are 24/min, and BP is 150/80 mmHg. PE shows 3+ pitting edema on LE, diffuse and scattered wheezes are heard bilaterally. Cardiac exam shows grade 2/6 pansystolic murmur heard best at the lower LSB, which increases on inspiration. The PMR is palpated in the sub-xiphoid area. S1 and S2 sound distant. Ab Exam shows a liver span of 14 cm. Which of the following is the likely dx?
A) Aortic stenosis
B) Cardiac amyloidosis
C) Cor pulmonale
D) CAD
E) primary pulm HTN

It should be C.
He is a long time smoker presenting with signs of right heart failure.
Also note that the murmur increases on inspiration which indicates a right side murmur...
COPD leads to pulmonary hypoxic vasoconstriction, that results in right ventricular hypertrophy and subsequent right heart failure.
 
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