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MudPhud20XX

MudPhud20XX

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Patient treated with fluphenazine presents the following day with a unilateral stiff , sore neck and back; What was the neurological reaction--which drug treatments might be appropriate?

a. acute dystonia: L-dopa
b. acute dystonia: diphenhydramine
c. acute dystonia: benztropine
d. tardive dyskinesia: reduce fluphenazine dosage
 
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MudPhud20XX said:
yeah B is the answer. man how did you know? can you pls explain?
Click to expand...

I don't know if you meant to quote Sailey instead of me or say C instead of B in your response, but either way both can do the job. I don't know the cost of benztropine, but it's Rx only and diphenhydramine is both cheap and OTC as well as relatively fast-acting (I'm sure we all have experience with this particular side effect). If the answer is B, then I see how diphendydramine is the appropriate answer when factoring in access/cost.
 
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We all know Benadryl has anticholinergic effects, dry mouth, urinary retention etc. you use this side effect to treat a very mild form of Dystonia (not Tardive dyskinesia) to treat this patient.
 
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Reasonable pharmacological step to treat tardive dyskinesia?
a. increase antipsychotic drug dose
b. add a tricyclic antidepressant to the drug regimen
c. add benztropine
d. start high dose diazepam
e. no pharmacological intervention is helpful after tardive dyskinesia is induced by antipyshotic treatment
 
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acetylcholine-blocking agents, despite being helpful in managing Parkinson's dz, should be avoided in pts with:
a. angle closure glaucoma
b. prostatic hyperplasia
c. pyloric stenosis
d. paralytic ileus
e. all of the above
 
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MudPhud20XX said:
Reasonable pharmacological step to treat tardive dyskinesia?
a. increase antipsychotic drug dose
b. add a tricyclic antidepressant to the drug regimen
c. add benztropine
d. start high dose diazepam
e. no pharmacological intervention is helpful after tardive dyskinesia is induced by antipyshotic treatment
Click to expand...

C.
 
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pathologyDO said:
C.
Click to expand...
It's actually D. not sure why though... anyone has an idea?

Reasonable pharmacological step to treat tardive dyskinesia?
a. increase antipsychotic drug dose
b. add a tricyclic antidepressant to the drug regimen
c. add benztropine
d. start high dose diazepam
e. no pharmacological intervention is helpful after tardive dyskinesia is induced by antipyshotic treatment
 
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MudPhud20XX said:
It's actually D. not sure why though... anyone has an idea?

Reasonable pharmacological step to treat tardive dyskinesia?
a. increase antipsychotic drug dose
b. add a tricyclic antidepressant to the drug regimen
c. add benztropine
d. start high dose diazepam
e. no pharmacological intervention is helpful after tardive dyskinesia is induced by antipyshotic treatment
Click to expand...

Lame. I wanted to write in F. switch to atypical. I guess it comes down to either you know that benzos can be used to treat TD, or by process of elimination.
 
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NeuroLAX said:
Lame. I wanted to write in F. switch to atypical. I guess it comes down to either you know that benzos can be used to treat TD, or by process of elimination.
Click to expand...

why would benztropine not be acceptable though? I just looked at our pharm lecture on this subject and he stated that:

Tx of extrapyramidal/TD symptoms you would use...

diphenhydramine
benztropine
trihexyphenidyl
 
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pathologyDO said:
why would benztropine not be acceptable though? I just looked at our pharm lecture on this subject and he stated that:

Tx of extrapyramidal/TD symptoms you would use...

diphenhydramine
benztropine
trihexyphenidyl
Click to expand...

Honestly, I don't have a good answer of precisely why. I just remember reading about it and writing down "switch to atypical, no anticholinergics" for TD treatment.
 
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pathologyDO said:
why would benztropine not be acceptable though? I just looked at our pharm lecture on this subject and he stated that:

Tx of extrapyramidal/TD symptoms you would use...

diphenhydramine
benztropine
trihexyphenidyl
Click to expand...

What? TD is due to increased sensitivity of D2 receptors. Anticholinergics would be useless. If withdrawing the antipsychotic doesn't resolve the TD, your only hope is a benzo for GABA potentiation. Don't group TD with EPS. The mechanism is not entirely the same as evidenced by the usual irreversibility of TD.
 
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a ten year old patient, being treated with ethosuximide for absence seizures, develops tonic-clonic seizures eight months later; choose LEAST appropriate drug for management of the new disorder.

A. phenytoin
B. valproate
C. carbamazepine
D. A&C
 
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Reason for short duration of action of i.v. diazepam;

A. pharmacodynamic tolerance
B. rapid metabolism
C. drug redistribution
D. A&B
 
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seminoma said:
What? TD is due to increased sensitivity of D2 receptors. Anticholinergics would be useless. If withdrawing the antipsychotic doesn't resolve the TD, your only hope is a benzo for GABA potentiation. Don't group TD with EPS. The mechanism is not entirely the same as evidenced by the usual irreversibility of TD.
Click to expand...

Alright, thanks. Just pointing out what our slides said.
 
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Effective in treating absence seizures:

A. ethosuximide
B. valproate
C. clonazepam
D. trimethadione
E. all of the above
 
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so midazolam is used in anesthesia or refractory status epilepticus. I get the anesthesia usage, but with short medazolam half life, i don't get its clinical usage for refractory status epilepticus, can anyone explain this? thank you.
 
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MudPhud20XX said:
so midazolam is used in anesthesia or refractory status epilepticus. I get the anesthesia usage, but with short medazolam half life, i don't get its clinical usage for refractory status epilepticus, can anyone explain this? thank you.
Click to expand...

I think that is the point actually. Status epilepticus is something that occurs acutely and you will thus treat it with a shorter acting drug, then afterwards treat with a longer acting drug that the patient can be prescribed for outpatient.
 
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A 51-year-old woman requires drug therapy for major depression. Her records indicate that she is currently being treated with guanethidine for hypertension. Which agent would be appropriate for the patient’s mood disorder but would most likely interfere with or antagonize her antihypertensive therapy?

a. carbamazepine
b. haloperidol
c. midazolam
d. nortriptyline
e. sertraline
 
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MudPhud20XX said:
A 51-year-old woman requires drug therapy for major depression. Her records indicate that she is currently being treated with guanethidine for hypertension. Which agent would be appropriate for the patient’s mood disorder but would most likely interfere with or antagonize her antihypertensive therapy?

a. carbamazepine
b. haloperidol
c. midazolam
d. nortriptyline
e. sertraline
Click to expand...

D
 
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correct...

Nortriptyline is indicated for major depression but would antagonize the effects of guanethidine. Nortriptyline is a tricyclic antidepressant (TCA). Like other TCAs, it blocks the reuptake process in presynaptic adrenergic nerve terminals. If this process does not occur, guanethidine cannot exert its antihypertensive effects, which are attributed to the gradual depletion of intraneuronal stores of norepinephrine. In addition to antagonizing the antihypertensive effects of guanethidine, TCAs antagonize the centrally mediated antihypertensive effects of α2-adrenergic receptor agonists such as methyldopa and clonidine.
 
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Can anyone help me with this q?

Which statement concerning the pharmacokientics of anti-seizure drug is accurate?
a. although ethosuximide has a half life of approximately 40h the drug is usually taken twice a day.
b. at high dose, phenytoin elimination follows first-order kinetics
c. the administration of phenytoin to patients in methadone maintenance programs has led to symptoms of opioid overdose, including reps depression
d. treatment with vigabatrin may reduce the effectiveness of oral contraceptrives
e. valproic acid may increase the activity of hepatic ALA synthase and the synthesis of porphyrins
 
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MudPhud20XX said:
Can anyone help me with this q?

Which statement concerning the pharmacokientics of anti-seizure drug is accurate?
a. although ethosuximide has a half life of approximately 40h the drug is usually taken twice a day.
b. at high dose, phenytoin elimination follows first-order kinetics
c. the administration of phenytoin to patients in methadone maintenance programs has led to symptoms of opioid overdose, including reps depression
d. treatment with vigabatrin may reduce the effectiveness of oral contraceptrives
e. valproic acid may increase the activity of hepatic ALA synthase and the synthesis of porphyrins
Click to expand...

A? Ethosuximide has a long-ish t1/2 and has significant GI side effects so it is dosed 2x per day.

B. zero order
C. phenytoin induces CYP, so if anything it would lead to withdrawal (not OD)
D. don't know about this one, but don't remember learning any relationship between vigabatrin and OCPs
E. Valproic acid isn't an inducer (vs phenytoin/phenobarb).
 
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seminoma said:
A? Ethosuximide has a long-ish t1/2 and has significant GI side effects so it is dosed 2x per day.

B. zero order
C. phenytoin induces CYP, so if anything it would lead to withdrawal (not OD)
D. don't know about this one, but don't remember learning any relationship between vigabatrin and OCPs
E. Valproic acid isn't an inducer (vs phenytoin/phenobarb).
Click to expand...
thanks. your right seminoma, god dang, what was I smoking?, it was too early in the morning lol!
 
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A young girl is being treated for a mass in her right kidney, which has been diagnosed as a Wilms tumor. Her treatment of chemotherapeutics was started and she has developed a peripheral neuropathy as a result of her medication. What chemotherapeutic was used that caused this adverse effect?
 
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pathologyDO said:
A young girl is being treated for a mass in her right kidney, which has been diagnosed as a Wilms tumor. Her treatment of chemotherapeutics was started and she has developed a peripheral neuropathy as a result of her medication. What chemotherapeutic was used that caused this adverse effect?
Click to expand...

Vincristine? Unless dactinomycin causes neuropathy too.. then dactinomycin.
 
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Which one(s) of the following statements is/are correct?

a. paroxetine is likely to exhibit more anticholinergic symptoms compared to fluoxetine norsertraline
b. sertraline is associated with a lower risk of adverse during interaction compared to fluoxetine or paroxetine
c. both
d. neither
 
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Buspirone::

a. is effective in treating depression
b. is cross-tolerant with benzodiazepine
c. does not produce significant levels of sedation
d. is a benzodiazepine
e. has a rapid onset of action
 
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least likely to cause orthostatic hypotension:
a. desipramine
b. sertraline
c. doxepin
d. tranylcypromine
e. amitriptyline
 
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MudPhud20XX said:
Buspirone::

a. is effective in treating depression
b. is cross-tolerant with benzodiazepine
c. does not produce significant levels of sedation
d. is a benzodiazepine
e. has a rapid onset of action
Click to expand...

C. Knowing that E is false is probably the most important thing to know about buspirone.

MudPhud20XX said:
least likely to cause orthostatic hypotension:
a. desipramine
b. sertraline
c. doxepin
d. tranylcypromine
e. amitriptyline
Click to expand...

B.
A, C, and E are TCA's which are known for their alpha-blocking properties, and D is an MAOI which also are characterized by orthostatic hypotension.
 
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effectiveness of local anesthetics when injected into infected tissue:
A. greater effect
B. reduced effect
C. no diff
 
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yup, as a result of reduced extracellular pH, more local anesthetic is in ionized form -- less likely to diffuse into the cell -- reduced effects. local anesthetics are weak base, so in infected tissue is acidic it will make the anesthetics as ionized form, thus leading to prolonging the onset.
 
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