Test your might!

[Depakote]

In the same vein as Allo's Name that Pathogen thread, let's get some good review going here. Anything on Step I is fair game.

A 37 year old male presents with a BP of 80/?. PT and PTT are elevated. Fibrinogen and Platelet count are decreased. D-Dimers are present. Peripheral blood smear reveals schistocytes as well as the following pathologic abnormality:

What is this patient's acute illness?
What is this patient's underlying illness?
Is there a specific abnormality associated with the underlying illness?
What must be done to treat this patient's underlying illness as not to aggravate the acute disease?

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[diosa428]

Yes so this young lady had a seizure. She is postictal on arrival, hence the confusion, and the hemiparesis is due to a phenomenon called Todd's Paralysis. Present in 10-15% or of all seizures. Lasts up to 48 hours.

Hey somedoc you are loving these intracranial hemorrhages, you should go into neurointerventional radiology! To have an epidural you would really need a higher energy injury to crack the skull and MMA in a young healthy patient.

She would still need a head CT for the LOC and to rule out any intracranial processes (tumor). Prolactin levels drawn immediately after the event correlate with seizures. I would also get a toxicology screen to rule out any drug use. EEG is useful in seizure patients, but will be negative unless its done DURING a seizure. Lastly, anti-epileptic treatment is not usually initiated on a first seizure, as most people will not have a second one. It is usually held until a second one occurs.

Good stuff, thanks

 

[SouthernSurgeon]

Good stuff, thanks

yeah, but if I'm remembering my step 1 studying right, that is nearly entirely beyond the scope of step 1...they'd only ever expect you to get to a "where is the lesion" type answer from that kind of vignette

 

[AllUpOnYoMama]

A 14-year-old fem comes to the physician because of a vaginal discharge. The discharge started about 2 months ago and is whitish in color. No odor. No complaints of itching, burning, or pain. The patient started breast development at 9 years of age and her pubertal development has proceeded normally to this point. She has not had her first menses and she is not sexually active. She has no medical problems. Examination is normal for a 14-year-old female. Microscopic examination of the discharge shows no evidence of pseudohyphae, clue cells, or trichomonads. diagnosis?

1-Bacterial vaginosis
2-Candida albicans
3-Trichomonas
4-HIV
5-Ovarian cyst
6-Physiologoic leukorrhea
7-Sphyillis
8-Pregnancy
9-Delayed maturation
10-Neisseria gonorrhea
11-Chlamydia trach

ans) #6. Physiologic leukorrhea can be seen during 2 different periods of childhood. Some female neonates develop a physiologic leukorrhea shortly after birth as maternal circulating estrogens stimulate the newborn's endocervical glands and vaginal epithelium. discharge in these neonates is often gray and gelatinous. Physiologic leukorrhea can also be seen during the months preceding menarche. During this time, rising estrogen levels lead to a whitish discharge not associated with any symptoms of irritation. This patient has a whitish discharge, no other symptoms, and she has had normal pubertal development up to this point. The discharge itself has no characteristics of infection. Therefore, physiologic leukorrhea is the most likely diagnosis. Bacterial vaginosis is not the most likely diagnosis in this patient because the discharge is not malodorous and there are no clue cells seen on microscopic examination of the discharge. Candida vulvovaginitis is not the most likely diagnosis because the discharge is not thick and white (or "cottage-cheese"-like) and the patient has no irritative symptomatology. Syphilis most often presents with a painless ulcer (called a chancre) or is found with serologic testing. A nonmalodorous, whitish vaginal discharge in a 12-year-old female who is not sexually active is almost certainly not evidence of syphilis.Trichomoniasis is also highly unlikely in this patient and the lack of trichomonads on the microscopic examination effectively rules out this diagnosis. Of the last choices, she says that she is not sexually active.

 

[Depakote]

A pre-med woman presents to your office. She is upset because she is studying immunology and she is concerned that should she conceive a child, her immune system will attack it. What do you tell her?

btw. I was going for someting about the decidual reaction here. pretty much got skipped.

 

[Depakote]

A 30 year old man presents to your clinic with a productive cough. He says he seems to "get these bugs all the time". You note purluent sputum. Aside from the recurrent respiratory infections, review of systems is normal except he states he and his wife have been trying to have a baby for some time now. They are considering seeing a fertility specialist.

Physical exam reveals bilateral basilar crackles and the point of maximum impulse is found to be the right 5th intercostal space.


What's going on here?

 

[44466]

Kartagener's Syndrome

Defective cilia leading to infertility (immotile sperm), chronic respiratory infections.

PMI is located in the 5th RICS due to situs inversitus which is associated with the disease.

 

[Mortal_Lessons]

A 30 year old man presents to your clinic with a productive cough. He says he seems to "get these bugs all the time". You note purluent sputum. Aside from the recurrent respiratory infections, review of systems is normal except he states he and his wife have been trying to have a baby for some time now. They are considering seeing a fertility specialist.

Physical exam reveals bilateral basilar crackles and the point of maximum impulse is found to be the right 5th intercostal space.


What's going on here?

Finding the apical impulse on the opposite side of what is considered normal (dextrorotation?), in addition to the possibility of male factor infertility (perhaps congenital bilateral absence of the vas deferens) and recurrent respiratory infections, brings to mind mucoviscidosis. I wonder if the patient has a mutation in the Cystic Fibrosis Transmembrane Conductance Regulator gene. Mutations in exon 509 are most common in CF, but this patient may have a milder mutation, resulting in less severe disease than full blown CF.

 

[SOUNDMAN]

Kartagener's, actually had this on my Step I exam as a question.

 

[Depakote]

Kartagener's Syndrome

Defective cilia leading to infertility (immotile sperm), chronic respiratory infections.

PMI is located in the 5th RICS due to situs inversitus which is associated with the disease.

 

[SouthernSurgeon]

Physical exam reveals bilateral basilar crackles and the point of maximum impulse is found to be the right 5th intercostal space.

That reminds me - the first time I ever successfully palpated a spleen was on the right side of a patient w/ complete situs AND myelofibrosis.

 

[Depakote]

That reminds me - the first time I ever successfully palpated a spleen was on the right side of a patient w/ complete situs AND myelofibrosis.

wow, now that I see it quoted... I'm awesome at grammar.

 

[thethom]

Finding the apical impulse on the opposite side of what is considered normal (dextrorotation?), in addition to the possibility of male factor infertility (perhaps congenital bilateral absence of the vas deferens) and recurrent respiratory infections, brings to mind mucoviscidosis. I wonder if the patient has a mutation in the Cystic Fibrosis Transmembrane Conductance Regulator gene. Mutations in exon 509 are most common in CF, but this patient may have a milder mutation, resulting in less severe disease than full blown CF.

I keep telling you guys, consider the patient as a whole. CF is classically a disease of the young, noone presents with it at 30.

 

[SouthernSurgeon]

I keep telling you guys, consider the patient as a whole. CF is classically a disease of the young, noone presents with it at 30.

It was diagnosed in a 60+ year old individual at my hospital.

A kid got diagnosed and they were doing a family genetic analysis, and realized one of the grandparents had it as well (one of the mild phenotypes - she had frequent respiratory illnesses and was pretty short but was still alive and well)

 

[thethom]

Your n=1. In fact, MOST cases of CF are diagnosed before 6 months of age. Common things occur commonly. Thats how you should approach medicine.

 

[SouthernSurgeon]

Your n=1. In fact, MOST cases of CF are diagnosed before 6 months of age. Common things occur commonly. Thats how you should approach medicine.

But not necessarily how you should approach boards. If you see something about sterility and frequent respiratory infection, you best at least think about CF, regardless of patient age.

 

[Captopril]

I'm gonna sound like a total n00b, but the stuff you guys are going over is freaking HARD. I just started studying a week or so ago, but am not giving my test for a long time (I'm a recently graduated IMG, so I have some time to study). Are all of these obscure diseases (e.g. Kartagener's) in the commonly used study material? I'm assuming most of this stuff is Path, which I haven't gotten to yet during my step 1 prep, but I don't remember learning any of this crap.

 

[thethom]

But not necessarily how you should approach boards. If you see something about sterility and frequent respiratory infection, you best at least think about CF, regardless of patient age.

Thats true, but I can def tell you from my experience on the Step 1 that acknowledging every part of the question (especially the age) definately helps rule out some of the answer choices. Takayasu's and Giant Cell Arteritis are both large vessel diseases, and can actually present in a very similar fashion clinically and histologically, but if the patient is presented as a 20 year old asian woman with amaurosis fugax then you know which one it'll be.

For Captopril, yeah these aren't that obscure, but for the most part, when you get to path you'll def slap your forehead and say "OH YEAHHH, I remember going over that that." Wait till you get into residency and all of a sudden you have to learn subtypes I-XIII of every disease...

 

[Pollux]

Hmm, this discussion kinda reminds me of a hilarious article I read before: "Stereotyping for the USMLE: How To Discriminate Your Way To The Top"

http://www.agraphia.net/zac-fact-10-bigot-your-way-to-success/

And trust me, it really works.

Captopril - yes, Kartagener syndrome is fair game for the boards.

 

[SomeDoc]

A 10 year old male is brought to the clinic with a chief complaint of abdominal pain and diarrhea. The parents state that the child has been constantly sick with "colds," and has been been repeatedly sick before with either bloody or watery diarrhea on different occasions, and "pus-filled" skin infections. Analysis of the patient's blood reveals a leukocytic phagocytic abnormality. A specific test (the result of which is negative as predicted by the physician) is carried out to confirm the diagnosis.

What is this?
What is the prototypical cause of the patient's symptoms?
What test will be negative in this patient?

 

[Depakote]

A 10 year old male is brought to the clinic with a chief complaint of abdominal pain and diarrhea. The parents state that the child has been constantly sick with "colds," and has been been repeatedly sick before with either bloody or watery diarrhea on different occasions, and "pus-filled" skin infections. Analysis of the patient's blood reveals a leukocytic phagocytic abnormality. A specific test (the result of which is negative as predicted by the physician) is carried out to confirm the diagnosis.

What is this?
What is the prototypical cause of the patient's symptoms?
What test will be negative in this patient?

Dude's got Chronic Granulomatous Disease (neuts can phagocytose but anything inside them that has catalase can survive within the phagocyte). So you get a lot of purulent infx including staph (staph has the staff to make catalase, thanks Clin Micro).

The test is the NTB test (nitroblue-tetrazolium <- had to look that up). If negative, the patient cannot reduce the NTB and has GGD.

 

[SomeDoc]

Dude's got Chronic Granulomatous Disease (neuts can phagocytose but anything inside them that has catalase can survive within the phagocyte). So you get a lot of purulent infx including staph (staph has the staff to make catalase, thanks Clin Micro).

The test is the NTB test (nitroblue-tetrazolium <- had to look that up). If negative, the patient cannot reduce the NTB and has GGD.

Can you think of what enzyme is most commonly deficient or defective in this patient?

 

[Mortal_Lessons]

Can you think of what enzyme is most commonly deficient or defective in this patient?

NADPH Oxidase

 

[SomeDoc]

NADPH Oxidase

 

[diosa428]

Why the diarrhea? Just more infxns?

 

[SomeDoc]

Why the diarrhea? Just more infxns?

Chronic Granulomatous ds. sufferers are prone to repeated infections of S. Aureus, Aspergillus, and E.coli. The diarrhea- either watery or bloody, are to indicate enteric infection by E.coli (by either ETEC or EHEC respectively).

 

[Richspiders07]

Hmm, this discussion kinda reminds me of a hilarious article I read before: "Stereotyping for the USMLE: How To Discriminate Your Way To The Top"

http://www.agraphia.net/zac-fact-10-bigot-your-way-to-success/

And trust me, it really works.

Captopril - yes, Kartagener syndrome is fair game for the boards.

... and Kartagener's is mentioned in First Aid

 

[Depakote]

A 23 year old man is dump in the ED by his friends. You are able to ascertain that he has consumed street narcotics. You have recently been informed by the police that a large batch of narcotics tainted with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective neurotoxin known to kill dopamine producing neurons of the substantia nigra, was seized. If this patient consumed the tainted narcotics, what symptoms will he exhibit? What pathway(s) will be disrupted? What treatments will be available?

 

[Captopril]

... and Kartagener's is mentioned in First Aid

Haven't cracked open FA yet (doing a refresher read of Kaplan lecture notes first), hence my naivete. I was just worried because I don't remember learning Kartagener's (and other things of that obscurity level) during school, but if the go-to sources like FA have it, then all is well.

Thanks for the heads up, Richspiders & Pollux.

 

[SomeDoc]

A 23 year old man is dump in the ED by his friends. You are able to ascertain that he has consumed street narcotics. You have recently been informed by the police that a large batch of narcotics tainted with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective neurotoxin known to kill dopamine producing neurons of the substantia nigra, was seized. If this patient consumed the tainted narcotics, what symptoms will he exhibit? What pathway(s) will be disrupted? What treatments will be available?

Good ol' ecstasy. Parkinsonism. Corpus striatum to globus pallidus externus/internus, subthalamus, and thalamus. Bromocriptine, amantadine, levodopa, selegiline, and two more drugs that I'll now have to look up.

 

[Depakote]

Good ol' ecstasy. Parkinsonism. Corpus striatum to globus pallidus externus/internus, subthalamus, and thalamus. Bromocriptine, amantadine, levodopa, selegiline, and two more drugs that I'll now have to look up.

Yup.

You wouldn't be expected to know anything about MPTP, but recognizing that the loss of dopamine producing neurons in the substantia nigra = parkinsons

(incidentally, MPTP was discovered accidentally in just the manner described in the vignette, it's a very good model for Parkinsons, IIRC)

 

[TracksuitsRock]

I'm gonna sound like a total n00b, but the stuff you guys are going over is freaking HARD. I just started studying a week or so ago, but am not giving my test for a long time (I'm a recently graduated IMG, so I have some time to study). Are all of these obscure diseases (e.g. Kartagener's) in the commonly used study material? I'm assuming most of this stuff is Path, which I haven't gotten to yet during my step 1 prep, but I don't remember learning any of this crap.

Don't worry...I swear it will come back to you. I felt like a total idiot when I started studying - trivia like this would have given me palpitations - but I actually relearned it (it's easier the second time!) and took the test - and now I am enjoying the brief honeymoon period before all the knowledge falls out of my head again.

 

[bluntdissector]

Fun to see some neuro cases, Todd's was nice! Although I'm not sure how common a (fairly complete) unilateral Todd's would be after a generalized seizure...Anyone?

Regarding the older case:

Whoa.. that should be chorea. (Ataxia=cerebellum and assoc. pathways)

Please note that it is neither. Chorea implies involuntary movement (as in Huntingtons or Sydenhams etc) whilst proper classic ataxia implies, as you said, cerebellar damage or associated tract damage. This patient is weak and hence her movement LOOKS ataxic (finger nose tests, etc). This is called 'ataxic hemiparesis', meaning that the 'ataxia' stems from her weakness!

 

[Sublimelvc]

Hey everybody, great info here. This site got me into medical school and is already providing insight into Step1.

I just took the self-assessment NBME 4 hr exam and was lying in bed last night mulling over some of the questions.

Is Cancer staging and grading fair game? For example, a young lady had NHL and they provided the pertinent PE and Radiographic findings and wanted us to stage it. There are so many different cancers and staging algorithms that I don't think I could ever know that!

 

[SomeDoc]

Fun to see some neuro cases, Todd's was nice! Although I'm not sure how common a (fairly complete) unilateral Todd's would be after a generalized seizure...Anyone?

Regarding the older case:



Please note that it is neither. Chorea implies involuntary movement (as in Huntingtons or Sydenhams etc) whilst proper classic ataxia implies, as you said, cerebellar damage or associated tract damage. This patient is weak and hence her movement LOOKS ataxic (finger nose tests, etc). This is called 'ataxic hemiparesis', meaning that the 'ataxia' stems from her weakness!

Whoops... looks you may be cross-linking cases. PT was long gone in the brain specimen case

 

[bluntdissector]

Nope! Don't think there was cross-linking!

The first paragraph (Todd's) was regarding the case of the teenager that was found unconscious (everyone jumped to stroke, which - and please take this in the best way possible - would have gotten you killed if you were on 'internal medicine', at least in my hospital...)

The ataxia/chorea was a response on your comment on the first page of the thread, regarding the old MCA. She can have 'ataxia' (ataxic hemiparesis), but I think chorea is unlikely.

Sorry, I know it's kinda out of line to comment so long after the case, I only found the thread now, will stay with it this time!

 

[Saladin MD]

Is Cancer staging and grading fair game? For example, a young lady had NHL and they provided the pertinent PE and Radiographic findings and wanted us to stage it. There are so many different cancers and staging algorithms that I don't think I could ever know that!

Very very very very unlikely that this would be tested on the real thing.

At most, you would just need to know what TNM stands for, that staging is more important than grading, etc. But not how to stage individual cancers! No way Jose!

 

[Sublimelvc]

Thanks Saladin!

There were plenty of questions where I was just like, really? Are you serious?

 

[thethom]

Hey Blunt, Todd's actually occurs in 13% of ALL seizures, and most commonly after GTC seizures.. Hope that helps.

 

[thethom]

Good ol' ecstasy. Parkinsonism. Corpus striatum to globus pallidus externus/internus, subthalamus, and thalamus. Bromocriptine, amantadine, levodopa, selegiline, and two more drugs that I'll now have to look up.

Hey someDoc, just a small correction. MDMA is ecstacy. MPTP is closer in structure to an opioid.

As for treatment, you can generally start with amantadine, in an effort to keep the patient off of levodopa. then levodopa/carbidopa (comes as a combo tablet) can be used.

Other options are tolcapone, entacapone (COMT inhibitors), pergolide, ropinorole, pramipexole. (not sure if I'm spelling these right, took pharm 3 years ago)...

And if I remember right from good ole Snell Neuroanatomy, lastly, pallidotomy can be useful, as well as deep brain stimulation of what I believe is the subthalamic nucleus.

 

[bluntdissector]

Hey Blunt, Todd's actually occurs in 13% of ALL seizures, and most commonly after GTC seizures.. Hope that helps.

Thanks. I found a cool article (where they also quote 13%) that states the paresis is normally contralateral to the epileptogenic zone. I would assume this is not the case in TRULY primary generalized seizures, but who knows! Probably won't be on the boards...

 

[thethom]

Yeah, understandably you'd expect excitotoxicity wherever the seizure occurred, and since GTCs are on both hemispheres, you'd expect a "bilateral Todds" in those cases, however this just goes to show how much we still don't know about the brain.

One thing to consider is that GTCs commonly originate in ONE hemisphere and then spread to both via the corpus callosum, this could explain the Todd phenomenon. Interestingly, corpus callosectomy (WOW) was once used to prevent GTC seizures, can't have one if it can't spread to the other hemisphere!

 

[Captopril]

...And if I remember right from good ole Snell Neuroanatomy...

Long live Richard S. Snell.

 

[Captopril]

Just saw Kartagener's in the first chapter of Kaplan Anatomy. Freak-out averted.

 

[Redrox]

Bilateral adnexal masses are palpated in a 65 year old Japanese woman. Biopsy results in tissue that stains positive for mucin.

What is the diagnosis?
What are two skin paraneoplastic lesions that can be seen with this condition?
Where should we palpate for a lymph node?
How did being Japanese affect her chances of this disease?
And just for fun, what is most likely her blood type?

 

[SomeDoc]

Bilateral adnexal masses are palpated in a 65 year old Japanese woman. Biopsy results in tissue that stains positive for mucin.

What is the diagnosis?
What are two skin paraneoplastic lesions that can be seen with this condition?
Where should we palpate for a lymph node?
How did being Japanese affect her chances of this disease?
And just for fun, what is most likely her blood type?

Sounds like a krukenbergs tumor- gastric adenocarcinoma mets to ovaries.
Wild guess RE her ethnicity- perhaps an increased risk of a specific mutation of the ERB
oncogene?
lymph nodes- check supraclavicle nodes... can't remember the name of these nodes... there was a specific name...

Not sure about the rest- will be keeping an eye out for the other responses.

 

[SomeDoc]

Virchow's nodes... i think that's what the supraclavicular nodal mets were called... .. but yeah, looking forward to what the answers to the rest are.

 

[Saladin MD]

Just saw Kartagener's in the first chapter of Kaplan Anatomy. Freak-out averted.

Kartagener's on the exam is like free points. Don't worry bro, it will all come to you near the end, God-Willing...I was having a major freak out just four days before the exam, right before I took the NBME and felt better right after it.

Seriously, you will learn so much in the next few months, God-Willing. I remember when I first started studying I was like "Prader-Willi wha!?" But now that's like kid stuff.

I just hope I retain this stuff in the long term...Well, I've finished reading half of the Step 2 book (Secrets), and it seems like the same old stuff, so I guess I'm getting the review I need in order to retain this stuff long-term.

 

[Saladin MD]

What is the diagnosis?

Gastric CA

What are two skin paraneoplastic lesions that can be seen with this condition?

Acanthosis Nigricans
Hmmm, can't think of a second one.

Where should we palpate for a lymph node?

Virchows node (left supraclavicular)
St Joseph Mary's nodule (umbilicus)

I don't think St Joseph Mary's nodule is a lymph node, just a metastasis, so maybe this is the answer to the previous question?

How did being Japanese affect her chances of this disease?

Japanese have like a fifty percent higher incidence of gastric CA, most likely due to diet, i.e. smoked foods?

And just for fun, what is most likely her blood type?

Type A. Remember: gAstric.

 

[SomeDoc]

Gastric CA

Acanthosis Nigricans
Hmmm, can't think of a second one.

Virchows node (left supraclavicular)
St Joseph Mary's nodule (umbilicus)

I don't think St Joseph Mary's nodule is a lymph node, just a metastasis, so maybe this is the answer to the previous question?

Japanese have like a fifty percent higher incidence of gastric CA, most likely due to diet, i.e. smoked foods?

Type A. Remember: gAstric.

Ah, that makes more sense than an ERB oncogene mutation. Smoked foods=nitrosamines.

Great tip re: "gAstric"

 

[tch001]

for the associated skin lesions, you can also get Leser Trelat sign - sudden appearance of seborrheic keratosis

also can get Blumer's shelf - intrperitoneal mets that can be felt on the rectal exam and Trousseu's sign - chronic thrombosis

I just studied this this afternoon

Gastric CA

Acanthosis Nigricans
Hmmm, can't think of a second one.

Virchows node (left supraclavicular)
St Joseph Mary's nodule (umbilicus)

I don't think St Joseph Mary's nodule is a lymph node, just a metastasis, so maybe this is the answer to the previous question?

Japanese have like a fifty percent higher incidence of gastric CA, most likely due to diet, i.e. smoked foods?

Type A. Remember: gAstric.