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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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You are performing a pediatric health screening and you see a 8 year old female patient. The patient is shown to have mild allopecia and a subtle tremor. You check liver enzymes and find ALT and AST are elevated. The patient's mother indicates that she has no allergies and is only taking one prescription "to help her with school", they had tried another drug but that one didn't work. No over the counter medications have been used and the patient is up to date on all vaccinations. Vitals are within normal limits and the patient appears cognitively intact.

What is the cause of the allopecia, tremor, liver enzyme elevation, and the patients academic difficulty?
If there are multiple pathologies at work. Explain.

Oy! Perhaps a drug that has side effects of allopecia, tremor, and elevated liver enzymes--Depakote(R)? It is an antiepileptic, but it can also be used for migraines and bipolar disorder.
 
How about hyperthyroidism, which would account for the alopecia, the tremor, and the lack of school performance (jitters, can't sit still, maybe?). Perhaps the T4 is elevated secondary to a decreased production of Thryoid Binding Globulin in the liver due to a Hep infection or Rotor's disease or something similarly mild.

I'm really looking forward to the answers, this one's a stumper.
 
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You are performing a pediatric health screening and you see a 8 year old female patient. The patient is shown to have mild allopecia and a subtle tremor. You check liver enzymes and find ALT and AST are elevated. The patient's mother indicates that she has no allergies and is only taking one prescription "to help her with school", they had tried another drug but that one didn't work. No over the counter medications have been used and the patient is up to date on all vaccinations. Vitals are within normal limits and the patient appears cognitively intact.

What is the cause of the allopecia, tremor, liver enzyme elevation, and the patients academic difficulty?
If there are multiple pathologies at work. Explain.

The tremor, liver enzyme elevations, and patient's academic/behavioral problems can be explained by the neuropsychiatric presentation of Wilson's disease, a copper storage disease. Because the patient was having difficulty in school as a result of her disease, she was placed on treatment to help with concentration. Perhaps the alopecia is a side effect of therapy...
 
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All good thoughts...

What was going through my mind when I wrote it:

(apparently I neglected to include, as I originally intended, that the child was obese... my bad :oops:, that would have helped with the differential)

The child was experiencing absence seizures (grades were low), teacher or doc picked up on it and they treated. I wanted to test the side fx of Depakote (valproic acid) so I just said that they failed the first line treatment (Ethosuximide).

We were taught that pts on Depakote can wind up "fat, bald shaky and yellow"... making the patient fat here really would have helped. Again, my bad. :smack:
 
Aww, c'mon Depakote, I wanted to see how many more incorrect and wildly unlikely diagnoses we could come up with. :)
 
A mother just delivered a baby which was complicated by ischemia and hemorrhage. A CT scan of the head shows signs of hemorrhage near the sella tursica.
1) what's the dx?
2) what should you give this patient immediately so that the head hemorrhage doesn't cause adverse affects? (After controlling the hypovolemia)
3) What is the TPR, Cardiac output, and LVEDV during her episode of hypovolemic shock compared to normal?
4) What will happen to her Resistance to Venous return and Right Atrial Pressure when she receives a blood transfusion?
5) After the mother's condition subsides, the baby starts to develop cyanosis and respiratory distress. What is this condition called? Give the pathology.
6) What could have prevented this baby's condition?
7) What is the baby's lung compliance, RV, and FEV1/FVC ration during her condition compared to normal?
8) What cells in the affected organ produce a substance which can treat the baby's condition? What is the additional role of these cells?

I guess I'll answer them. lol
1) Sheehan's syndrome
2) Glucocorticoids and Thyroid hormones (T4 analogue). As these have the most adverse effects when in low quantities.
3) TPR would be high (to get blood to the peripheries), Cardiac Output would be low (low blood volume hence low preload), and LVEDV would be low in hypovolemic shock.
4) RVR should decrease when blood tranfusion is given (expands the venules due to more blood volume). And Right Atrial Pressure should be increased since you have more blood volume. Need to be increased so that not a whole lot of blood gets to the right atrium (or theheart)
5) Infant Respiratory Distress Syndrome of course. Hyaline membrane change. Destruction of the alveolar wall.
6) corticosteroids (increases surfactant production)
7) Infant RDS I would think is a restrictive lung dz since it affects the alveolar wall.
So, lung compliance would be low, RV should be low, and FEV1/FVC should be greater than 80%. (or greater than normal)
8) type II pneumocytes. They also play a role in regenrating the alveoli and interstitial lung tissue.

Alright. I think that's it!
 
A mother brings her twin sons in for a checkup:

achondroplasia1.jpg


Diagnosis?
Potential means of inheritance?
What is the defective gene?
How does the mutant gene cause the disease?
The mother inquires about growth hormone supplementation therapy for her child. Would this be useful?

Bonus:
How many chorion(s), amnion(s) and placenta(s) for these did these twins have in utero?
 
A mother brings her twin sons in for a checkup:

Diagnosis?
Potential means of inheritance?
What is the defective gene?
How does the mutant gene cause the disease?
The mother inquires about growth hormone supplementation therapy for her child. Would this be useful?

Bonus:
How many chorion(s), amnion(s) and placenta(s) for these did these twins have in utero?

1) Achondroplasia
2) AD
3) Messes up some growth factor ?
4) No

Since only one kid is affected these are fraternal/dizygotic twins, hence all these components are separate

p.s. Speaking of dwarves...anyone see "In Bruges".....awesome movie :)
 
Patient A is a 45 year old woman presenting for treatment of painful inflamed joints. Antibodies against the Fc portion of IgG are detected in her serum.

Patient B is a 38 year old HIV positive man presenting with a painful esophageal fungal infection.



Both of these patients will receive medications that target very similar pathways (different drugs), name them and the pathway.
What is the therapeutic mechanism shared by these drugs?
 
Patient A is a 45 year old woman presenting for treatment of painful inflamed joints. Antibodies against the Fc portion of IgG are detected in her serum.

Patient B is a 38 year old HIV positive man presenting with a painful esophageal fungal infection.



Both of these patients will receive medications that target very similar pathways (different drugs), name them and the pathway.
What is the therapeutic mechanism shared by these drugs?


A has rheumatoid arthritis, since its obviously not indomethicin, ill go with colchicine - inhibits microtubule function

Gresiofluvin is an antifungal drug also inhibit microtubule function.

I am guessing that this is what you are referring, but both are non first aid uses of the drugs!
 
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A has rheumatoid arthritis, since its obviously not indomethicin, ill go with colchicine - inhibits microtubule function

Gresiofluvin is an antifungal drug also inhibit microtubule function.

I am guessing that this is what you are referring, but both are non first aid uses of the drugs!

Actually, I'm going to differ from your latter part. The former part is right; Pt A has rhematoid and B probably has esophageal candidiasis secondary to immunosuppression via HIV. Tx for Pt A would be Methotrexate and Pt B would be TMP-SMX. Methotrexate inhibits dihydrofolate reductase, inhibiting reduction of nucleotide precursors that ultimately will downregulate DNA synthesis in leukocytes, while TMP-SMX inhibits dihydrofolate reductase and dihydropteroate synthase (something like that), which inhibits the incorporation of PABA into candida. The pathways are basically DNA synthesis (purine?) and have similar ends but differ on substrates. Common target is DHFR.
 
Actually, I'm going to differ from your latter part. The former part is right; Pt A has rhematoid and B probably has esophageal candidiasis secondary to immunosuppression via HIV. Tx for Pt A would be Methotrexate and Pt B would be TMP-SMX. Methotrexate inhibits dihydrofolate reductase, inhibiting reduction of nucleotide precursors that ultimately will downregulate DNA synthesis in leukocytes, while TMP-SMX inhibits dihydrofolate reductase and dihydropteroate synthase (something like that), which inhibits the incorporation of PABA into candida. The pathways are basically DNA synthesis (purine?) and have similar ends but differ on substrates. Common target is DHFR.


Patient B would probably get nystatin or an azole to actually treat the esophageal candiasis but if they've got it, that would be considered and AIDs defining illness and they'd need pneumocystis prophylaxis which would indicate a need for TMP-SMX which works through the mechanism you described.

:thumbup:
 
A 24 year old man is brought in to the ED by his friends. They were hiking in the desert when the man was stung by a scorpion several hours ago. The friends managed to catch the scorpion in a lunch-container and bring it to the ED as well:

ttrinitatis.jpg

An ED staffer identifies the scorpion as Tityus trinitatis.

The patient complains of severe abdominal pain which seems to go all the way through to his back and he also complains of significant nausea.

What do you suspect in this patient?
What labs or tests can you do to confirm the diagnosis?
What complications are you concerned about?
 
A 24 year old man is brought in to the ED by his friends. They were hiking in the desert when the man was stung by a scorpion several hours ago. The friends managed to catch the scorpion in a lunch-container and bring it to the ED as well:

ttrinitatis.jpg

An ED staffer identifies the scorpion as Tityus trinitatis.

The patient complains of severe abdominal pain which seems to go all the way through to his back and he also complains of significant nausea.

What do you suspect in this patient?
What labs or tests can you do to confirm the diagnosis?
What complications are you concerned about?

-Acute pancreatitis.
-Serum amylase and lipase can help confirm your suspicion. CT is the preferred imaging modality for the pancreas and can help you assess the patient's condition.
-The sequelae and potential mortality directly related to a severe acute pancreatic episode is particularly concerning.
 
-Acute pancreatitis.
-Serum amylase and lipase can help confirm your suspicion. CT is the preferred imaging modality for the pancreas and can help you assess the patient's condition.
-The sequelae and potential mortality directly related to a severe acute pancreatic episode is particularly concerning.

Acute Pancreatitis, check. :thumbup:

I agree that the complications are bad. Anyone want to expound on what they might be?
 
a 56 yr old man is complaining of heart arrythmias, excessive daytime sleepiness, gastroparesis and sleep apnea. his wife brings him to your clinic although he is reluctant to seek assistance. you notice facial muscle weakness along with ptosis. he also has some generalized upper and lower muscle weakness. the man has some cognitive impairments.

what is the mechanism for acquiring this disease?
what is the treatment?
how common is it?

a man comes to your clinic complaining of muscle weakness. he tells you that sometimes his hands "twitch". you perform a motor and sensory tests and note that his sensory tests are normal but he has hyperreflexia, a positive babinski sign and generalized musle fasciculations. you order an MRI

What does the MRI show?
what is the treatment for the disease?
 
a woman (how come men get all the diseases...) presents to your clinic with dance-like movements. she thrusts her tongue out continously. she has trouble remembering stuff and flat affect.

on what chromosome is the gene responsible for this disorder found?

no googling!!!! i came up with a mnemonic that i'm really excited about.
 
a 56 yr old man is complaining of heart arrythmias, excessive daytime sleepiness, gastroparesis and sleep apnea. his wife brings him to your clinic although he is reluctant to seek assistance. you notice facial muscle weakness along with ptosis. he also has some generalized upper and lower muscle weakness. the man has some cognitive impairments.

what is the mechanism for acquiring this disease?
what is the treatment?
how common is it?

Myotonic dystrophy, autosomal dominant, CTG repeats
no treatment
most common muscular dystrophy in adults

a man comes to your clinic complaining of muscle weakness. he tells you that sometimes his hands "twitch". you perform a motor and sensory tests and note that his sensory tests are normal but he has hyperreflexia, a positive babinski sign and generalized musle fasciculations. you order an MRI

What does the MRI show?
what is the treatment for the disease?


Amyotrophic Lateral Sclerosis
nothing on MRI
no cure but treatment is Riluzole
 
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