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Depakote

Pediatric Anesthesiologist
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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:

58346542.jpg


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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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:

58346542.jpg


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?

Great idea Dep. I was itching to post some good pathology vignettes in the name that pathogen thread, and am glad you started this.

OK, so here goes...
DIC
Hereditary spherocytosis
Ankryn/Spectrin deficiency/defect
Splenectomy
 
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:

58346542.jpg


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?

Ballerina skirting? Mono?
 
1) DIC
2) M3 AML
3) t (15,17)
4) Prophylactic Heparin to prevent coagulation caused by release of procoagulants from lysis caused by cytotoxic drugs used to treat AML
 
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1) DIC
2) M3 AML
3) t (15,17)
4) Prophylactic Heparin to prevent coagulation caused by release of procoagulants from lysis caused by cytotoxic drugs used to treat AML

same... however throw some retinoic acid in there for treatment
Now we've got it. :thumbup:

except how does retinoic acid prevent DIC??

In M3 AML the Retinoic acid (ATRA) causes the immature promyelocytes to differentiate fully. If you give cytotoxic drugs before the cells differentiate they will lyse and the spillage of their contents can worsen the DIC.
 
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:

58346542.jpg


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?


Nice F-aggot Cell!!!!! (I just had to test the censor program with this medically acceptable description...guess you could also call them Auer rod cells)
 
A 55 year old man presents to the ER complaining of the recent onset of a headache and nausea. On physical exam his skin appears flushed.

His Oxygen-Hemoglobin dissociation curve is presented below (red) compared to a normal curve (blue):
shiftedcurvecopy.jpg


What is the most likely cause of this man's illness?
How would you treat it?
 
A 55 year old man presents to the ER complaining of the recent onset of a headache and nausea. On physical exam his skin appears flushed.

His Oxygen-Hemoglobin dissociation curve is presented below (red) compared to a normal curve (blue):
shiftedcurvecopy.jpg


What is the most likely cause of this man's illness?
How would you treat it?

The physical findings suggest CO poisoning, but the O2 dissosc. curve does not suggest it (in CO poisoning, O2 max saturation would be low). The curve is consistent w/ fetal Hb high O2 affinity, I'm going to go with Beta Thalassemia. Tx. w/ transfusion.

He could also be in metabolic or respiratory alkalosis stemming from a variety of causes. In this case I would administer acetazolamide.
 
The physical findings suggest CO poisoning, but the O2 dissosc. curve does not suggest it (in CO poisoning, O2 max saturation would be low). The curve is consistent w/ fetal Hb high O2 affinity, I'm going to go with Beta Thalassemia.

Or I just screwed up drawing the left shift. It was supposed to be CO poisoning.
 
I'm gonna say Carbon Monoxide poisoning. 100% O2 via non-rebreather or hyperbaric oxygen. Blood gas carboxyhemoglobin levels to verify. CXR to assess concurrent lung injury.

Unfortunately in real life, you won't always see the skin flushing that they will give you on the boards...

-T
 
Ok, I didn't screw up as much as I thought I did...

http://www.coheadquarters.com/cohaldane1.htm

These plots show the effect of carbon monoxide on the oxygen dissociation curve, the so-called Haldane Effect. I = 0% COHb, II = 10% COHb, III = 25% COHb, IV = 50% COHb, V = 75% COHb. As more CO attaches to hemoglobin, the oxygen dissociation curve for that hemoglobin that can still carry oxygen shifts to the left and comes to take on a hyperbolic shape rather than a sigmoidal shape

You can still get a high saturation of the Hb capable of binding O2, that which hasn't bound CO. (that's what the curve is showing)
 
I'm gonna say Carbon Monoxide poisoning. 100% O2 via non-rebreather or hyperbaric oxygen. Blood gas carboxyhemoglobin levels to verify. CXR to assess concurrent lung injury.

Unfortunately in real life, you won't always see the skin flushing that they will give you on the boards...

-T
:thumbup:
 
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Damn you posted the answer as I was typing it. BTW Depakote, you're right, and the dissociation curve is fine, its not like you get an oxygen dissociation curve in real life anyway lol.

Also SomeDoc, a 55 year old male with thalassemia and flushing of the skin? Treat the patient as a whole, not just the "labs".
 
Damn you posted the answer as I was typing it. BTW Depakote, you're right, and the dissociation curve is fine, its not like you get an oxygen dissociation curve in real life anyway lol.

Yeah, but just trying to mix it up and throw in some physio instead of straight path.
 
Here's a less straightforward one...

The brain of a 79 year old female is examined at autopsy:
2mca.jpg


Which vessel was involved in this lesion?
Is this a recent or old lesion? How do you know?
What deficits might be associated with this lesion?
Is this the direct cause of death?
 
Here's a less straightforward one...

The brain of a 79 year old female is examined at autopsy:
2mca.jpg


Which vessel was involved in this lesion?
Is this a recent or old lesion? How do you know?
What deficits might be associated with this lesion?
Is this the direct cause of death?

Right MCA
Old lesion (cavity and no early edema)
Contralateral upper limb and lower face paresis, loss of sensation contralterally, Wernikes (receptive) aphasia, possibly Broccas (though to me the location looks more like Wernikes)
Since it is old nt the direct cause of death.
 
Right MCA
Old lesion (cavity and no early edema)
Contralateral upper limb and lower face paresis, loss of sensation contralterally, Wernikes (receptive) aphasia, possibly Broccas (though to me the location looks more like Wernikes)
Since it is old nt the direct cause of death.

Also, could be some vision loss (like a left quandrantopia) if it hits those fibers in the temporal lobe
 
Right MCA
Old lesion (cavity and no early edema)
Contralateral upper limb and lower face paresis, loss of sensation contralterally, Wernikes (receptive) aphasia, possibly Broccas (though to me the location looks more like Wernikes)
Since it is old nt the direct cause of death.

Above, and adding that wernicke's in this case will be rare b/c wernicke's area is usu on the left hemisph. Also potentially contralat ataxia (potential globus pallidus involvement- if lesion is deep enough medially)
 
Above, and adding that wernicke's in this case will be rare b/c wernicke's area is usu on the left hemisph. Also potentially contralat ataxia (potential globus pallidus involvement- if lesion is deep enough medially)

ahh very good point about the language centers !!!:)
My non sleeping brain isin't that sharp right now;)
 
Yes the above posters are correct for the most part. As mentioned, this would NOT result in a wernike's or broca aphasia (or global aphasia since both are gone), since those centers are on the left side. They however could result in what is known as receptive and/or expressive dysprosody. The corresponding "wernikes" and "brocas" areas on the right hemisphere allow the patient the ability to respectively perceive or express inflections/tone/mood in speech. Without these, speech would be monotone and the patient would not be able to appreciate "mood" in speech.

Lastly as mentioned above, this is not an acute cause of death. Stroke patients like this can end up debilitated, bedridden, and just as Sam Shem wrote in his novel "The House of God," gomers never die... :p

-T
 
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Above, and adding that wernicke's in this case will be rare b/c wernicke's area is usu on the left hemisph. Also potentially contralat ataxia (potential globus pallidus involvement- if lesion is deep enough medially)

Whoa.. that should be chorea. (Ataxia=cerebellum and assoc. pathways)
 
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?
You have anti-kell, anti-D, and anti-duffy antibodies in your blood. This is the first time I have ever seen all three in one person. Your child is proper fuked.
 
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
 
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

6-Physiologic leukorrhea-sometimes occurs prior to first period and is a sign of puberty (ref: Wiki)
 
Sounds like physiologic discharge(leukorrhea). Of course in real life you'd swab for GC/Chlam anyways(pts always lie about sex). Clear microscopy rules out candidal vaginosis, trich, and gardnerella.
 
20 year old female student with no PMHx is found by her roommate lying unconscious on the floor in the room. On arrival to ER she is awake, stable vitals, afebrile, but is confused and unable to move the left side of her body. This whole process has never happened to her before. What is the diagnosis and what do you do?
 
20 year old female student with no PMHx is found by her roommate lying unconscious on the floor in the room. On arrival to ER she is awake, stable vitals, afebrile, but is confused and unable to move the left side of her body. This whole process has never happened to her before. What is the diagnosis and what do you do?

R. MCA thrombus/thromboembolism. Administer heparin. Check oral contraception pill status, and familial Hx of cardiovascular ds. to r/o hereditary hypercholesterolemia.
 
So even IF it was a stroke, what if it was a hemorrhagic stroke and you just gave heparin without checking a head CT(the FIRST thing do do when you suspect stroke)... Think again, how common is a stroke in a 20 year old. Diagnose the patient as a whole.
 
R. MCA thrombus/thromboembolism. Administer heparin. Check oral contraception pill status, and familial Hx of cardiovascular ds. to r/o hereditary hypercholesterolemia.


In an older patient, if an ischemic stroke is confirmed (no hemorrhage on CT) then first step would be to give tPa thrombolysis (if symptoms are less than 3 hours old and no other absolute contraindications (look em up). If >3 hours, tPa is no longer effective and heparinization to prevent further clot is indicated. Of note, heparin does NOT dissolve clot, only prevents further formation.
 
Other possibilities in the differential include:

Multiple Sclerosis- CT would be helpful here

MS is a good thought considering the gender and age of the patient, however the ACUITY of the situation suggests otherwise.

Of note, to diagnose MS you really need an MRI-flair image, and then a specific type of banding on the CSF electrophoresis.
 
MS is a good thought considering the gender and age of the patient, however the ACUITY of the situation suggests otherwise.

Of note, to diagnose MS you really need an MRI-flair image, and then a specific type of banding on the CSF electrophoresis.

good to know. Just getting into the details of neuropath now. :thumbup:
 
Sounds like physiologic discharge(leukorrhea). Of course in real life you'd swab for GC/Chlam anyways(pts always lie about sex). Clear microscopy rules out candidal vaginosis, trich, and gardnerella.

On the boards, yes. In real life, wetprep can be negative in up to ~50% of vaginal yeast infections.
 
20 year old female student with no PMHx is found by her roommate lying unconscious on the floor in the room. On arrival to ER she is awake, stable vitals, afebrile, but is confused and unable to move the left side of her body. This whole process has never happened to her before. What is the diagnosis and what do you do?

Good points.

CT to r/o hemorrhage/occlusion of MCA, or right hemispheral epidural hematoma (patient may currently be at a lucid interval) arising from r. temporal artery damage from a fall secondary to a seizure.
 
I like it.

Fall (unknown cause, seizure?)-> epidural hematoma (MMA artery rupture) causing current symptoms-> possible subfalcine herniation, watch for ipsilateral symptoms as herniation progresses (uncal herniation-> compression against tentorium cerebelli)-> if untreated, rupture of basillar artery branches to pons will cause death.
 
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Good points.

CT to r/o hemorrhage/occlusion of MCA, or right hemispheral epidural hematoma (patient may currently be at a lucid interval) arising from r. temporal artery damage from a fall secondary to a seizure.

AHA the last word in your post is getting closer!
 
20 year old female student with no PMHx is found by her roommate lying unconscious on the floor in the room. On arrival to ER she is awake, stable vitals, afebrile, but is confused and unable to move the left side of her body. This whole process has never happened to her before. What is the diagnosis and what do you do?

The two most salient differentials in this patient are syncope or seizure. Her confusion and left hemiparesis argue in favor of seizure. The post-ictal unilateral weakness (Todd paralysis) suggests a focal brain lesion as the cause and calls for further investigation. Perhaps an MRI?
 
General atonic seizure--> fall-->r. MMA rupture-->r. hemisphere epidural hematoma-->l.upper/lower hemiparesis.
 
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.
 
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