Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
51 Cards in this Set
- Front
- Back
|
A 60 y/o male w/COPD is given ipatropium as part of his therapeutic regimen. What is the MOA of ipatropium?
a.) inhibition of airway muscarinic receptors b.) inhibition of 5-lipoxygenase c.) breakdown of mucus d.) inhibition of mediator release e.) inhibition of phosphodiesterase f.) activation of β-adrenergic receptors |
inhibition of airway M-R's
Ipatropium is a quaternary derivative of atropine, which means it is not absorbed into the CNS, and theoretically, devoid of the dizziness & delirium of a tertiary anti-muscarinic. Remember how atropine makes you hot as a hare, dry as a bone, red as a beet, blind as a bat & mad as a hatter!!! |
|
|
A 1 y/o male develops decreased breath sounds, and wheezing during a febrile episode, which is relieved by albuterol. What is the MOA of albuterol?
a.) Inhibition of airway muscarinic receptors b.) inhibition of 5-lipoxygenase c.) breakdown of mucus d.) inhibition of mediator release e.) inhibition of phosphodiesterase f.) activation of β-adrenergic receptors |
activation of beta adrenergic R
Albuterol is a SABA. It is effective in obtaining immediate relief and is delivered by inhalation in acute episodes of bronchospasm. Its action may last up to fours hours. Salmeterol is a long acting β-adrenergic agonist that can be taken orally and is useful for prophylaxis. Although β-adrenergic agonists may be delivered orally, adverse effects are minimized when used by inhalation. |
|
|
A 10 y/o w/allergy induced asthma is treated w/cromolyn. What is the MOA of cromolyn?
a.) inhibition of airway muscarinic receptors b.) inhibition of 5-lipoxygenase c.) breakdown of mucus d.) inhibition of mediator release e.) inhibition of phosphodiesterase f.) activation of β-adrenergic receptors |
inhibition of mediator release
Cromolyn inhibits degranulation of mast cells. Also inhibits degranulation of eosinophils, imagine that. |
|
|
A 35 y/o patient of yours if finally going to quit smoking. You manage his asthma with fluticasone and theophylline (he did not want to add salmeterol when his fluticasone proved inadequate by itself). Anyway, in counseling him through this you must
a.) Increase his dose of theophylline b.) Increase his dose of theophylline and warn him to avoid any nicotine patches, gums or other supplements on this new higher dose c.) Decrease his dose of theophylline d.) Decrease his dose of theophylline and warn him to avoid any nicotine patches, gums or other supplements on this new higher dose e.) Discontinue his fluticasone, he will no longer need it since smoking is the most important factor in managing asthma |
decrease his dose of theophylline
Theophyline is most famous for the many factors that influence its metabolism. Children between 1 & 9 y/o best metabolize the drug. This is only drug I can think of right now where a 20 pound kid might get a bigger dose than a 200 pound trucker, counterintuitive & very testable. Other things that increase the metabolism of the drug include the cigarette smoke, food cooked over charcoal, some anti-convulsant drugs & rifampin. It is important to note that it is not the nicotine in cigarettes with which the theophylline metabolism depends, it is rather linked to the burning of the cigarette. Smoking is not the most important factor in managing asthma, since not all asthmatics smoke, yet it is the most important factor in managing COPD, since in the vast majority of cases, COPD is linked to cigarette smoke. |
|
|
Some parents are concerned that steroids may stunt their asthmatic child’s growth. Which of the following should not be part of your argument for the use of steroids in the treatment of asthma?
a.) The dose of inhaled corticosteroids used in asthma may cause hoarseness, dysphagia and oral candidiasis, but is not enough to cause stunted growth. b.) Hypoxia stunts growth c.) Steroids never stunt growth, that is a myth d.) Inhaled corticosteroids are the drug of choice in the treatment of any sort of persistent asthma e.) Asthma is best managed with less frequent dosing of the more potent ICS |
steroids never stunt growth that is a myth
Steroids in really high doses definitely have the potential to stunt growth. It is important to tell parents that these are the same steroids that account for Arnold Schwarzenegger’s big jaw and wide spaced teeth. These are the cornerstone in treating any sort of persistent asthma. |
|
|
Which of the following is true regarding anticholinergics, such as ipatropium bromide?
a.) Drug of choice as a scheduled med in COPD b.) Drug of choice to be added as a scheduled med to ICS in asthma c.) May cause sweating, salivation & bradycardia d.) Ipatropium gets into the CNS, so overdose is characterized by seizures and dysrhythmias e.) They compete with Ach receptors to decrease cAMP, to decrease vagal tone and bronchodilate |
durg of choice as a scheduled med in COPD
Ipatropim & tiotropium are not used too often in asthma, but they are the DOC in the scheduled management of COPD. In treating COPD: stop smoking -> add albuterol -> tiotropium -> add LABA or SABA (scheduled) -> add theophylline -> add steroids -> pulmonary rehab, consider surgical removal of blown out alveoli |
|
|
When treating asthma, LABA should be used
a.) As a rescue medication b.) As a first line agent in monotherapy of any persistent asthma c.) As a first line agent in monotherapy of severe peristent asthma d.) Only in COPD e.) As an addition to ICS, when patient still must use a rescue inhaler twice a week or more |
as an addition to ICs, when pt still must use a rescue inhaler twice a week or more
If you are going to get anything out of this lecture, remember that treating persistent asthma begins with an ICS. If that is not enough, we add a LABA. It is preferential to add a LABA to a low dose of ICS, because it potentiates the effect of the steroid. LABAs are too long acting to be rescue meds, are never first line as monotherapy and don’t really have too much of an effect in COPD as compared to asthma. |
|
|
COPD includes (more than one may apply)
a.) Emphysema, a disorder characterized by a loss of alveolar compliance b.) Chronic bronchitis, a disorder characterized by hypertrophy of mucus glands in the bronchus c.) Presents with the same symptoms as asthma, except that it is often irreversible. d.) The growth of lung cancers into the alveoli, accounting for their loss of elasticity e.) Diagnosed with spirometry |
chronic bronchitis (hypertrophy of mucus glands in bronchus)
presents with same symptoms as asthma except often irreversible diagnosed w/spirometry Classically, COPD encompasses emphysema & chronic bronchitis. One person may tend to have a COPD more characteristic of emphysema (pink puffer), while his smoking buddy might have a COPD more characteristic of chronic bronchitis (blue bloater), and in both cases, the diagnosis is COPD. Bronchiectasis is kind of on the spectrum of emphysema, in that bronchiectasis refers to loss of elasticity at the bronchiole level, while emphysema refers to the loss of elasticity of the alveoli and structures supporting the alveoli, like tethers and blood vessels. COPD has nothing to do with CA, but CA is another sequelae of tobacco exposure. |
|
|
In the treatment of asthma, as physicians we aim for all of the following except
a.) A near normal level of activity b.) Prevent airway remodeling, and thereby prevent the fibrosis that makes airway obstruction irreversible c.) Using a rescue inhaler < 4x a week d.) Near normal PFTs e.) Eliminating symptoms |
using a rescue inhaler < 4X/wk
A patient is not considered well manage if they are using their rescue inhaler 4x a week or more, we need it used less than twice a week. |
|
|
In the treatment of COPD, the most important factor is
a.) Smoking cessation b.) Beginning with ICS c.) The decision to never use a short burst of steroids in controlling outbreaks d.) Adding theophylline to the use of O2 therapy in the initial management of the disease |
smoking cessation
|
|
|
In diagnosing myasthenia gravis, edrophonium if often used. The following two drugs have the same MOA, but are longer lasting, and are therefore, preferred for treatment of this condition.
a.) physostigmine & rivastigmine b.) physostigmine & pyridostigmine c.) rivastigmine & donepezil d.) neostigmine & rivastigmine e.) neostigmine & pyridostigmine |
neostigmine and pyroidostigmine
All of the above listed drugs are reversible inhibitors of acetylcholine esterase. Neo & Pyrido work well in the treatment of MG, and reversal of a neuromuscular blockade, while pyridostigmine is also used as a prophylactic agent for nerve gas. Rivastigmine & donepezil are commonly used for the treatment of Alzheimer’s disease. Physostigmine is an antidote for antimuscarinic poisoning. |
|
|
This drug is often used in pulmonary function testing. Other drugs of its class are used in the treatment of gastroparesis, urinary retention, glaucoma & xerostomia.
a.) bethanechol b.) methacholine c.) rivastigmine d.) ipatropium e.) pilocarpine |
methacholine
Remember the methacholine challenge? Methacholine is a direct muscarinic agonist, like bethanechol, carbachol and pilocarpine. This is given to suspected asthmatics before performing spirometry, since the airways of asthmatics are out of balance & more apt to bronchoconstrict, giving them an increased sensitivity to methacholine. |
|
|
In treating COPD, we often use muscarinic antagonists to make the airway less vagal and promote bronchodilation. Other drugs in this class are used in the treatment of motion sickness, Parkinsons and irritable bowel syndrome. They include
a.) Benztropine in the treatment of Parkinsons b.) Linezolid in the treatment of MRSA c.) Rivastigmine in the treatment of Alzheimers d.) Sildenafil in the treatment of ED |
benztropin in the tx Parkinsons
|
|
|
Fertile Myrtel comes to your office to announce that she is pregnant! She has a long hx of MDD (major depressive disorder), and has been taking fluoxetine at full doses for the past 7 months, with full remission of symptoms. You advise her too
a.) Discontinue the fluoxetine immediately, SSRIs are associated with cardiac teratogenicity. b.) Discontinue the fluoxetine and begin electroconvulsive therapy. c.) Remain on the fluoxetine, full dose, depression would be more detrimental to the fetus than would this SSRI. d.) Remain on the fluoxetine, but begin tapering dose during the 3rd trimester to avoid a serotonin withdrawal in the child. e.) Remain on the fluoxetine, but immediately decrease to half dose |
Remain on the fluoxetine, but begin tapering dose during the 3rd trimester to avoid a serotonin withdrawal in the child.
Remember that it has not been assessed how antidepressants ultimately the behavior of an unborn child. Yet, fluoxetine has a good safety record. If Ms. Myrtle has been on paroxetine, you would want to switch to fluoxetine. I am not sure how you would manage her if she had been on a TCA. But, if this depression was new onset, the psychiatrists who you will do your clerkship with M3 would opt for electroconvulsive therapy. |
|
|
A patient comes to your office with complains of depressed mood, hypersomnia, decreased appetite and difficulties with concentration. He has been this way for at least 2 mos, and cannot seem to think of anything that may have started this. What should your initial move be?
a.) Begin a trial of SSRI, this is the initial drug of choice in depression b.) Began a trial of SSRI along with a hypnotic to decrease the chance of suicide c.) Inquire about a hx of substance abuse, run a urinalysis for THC if marijuana use is suspected, run blood work to assess TSH and free T4 levels d.) Tell him to pull up his skirt, grab his huevos and get happy! |
c.) Inquire about a hx of substance abuse, run a urinalysis for THC if marijuana use is suspected, run blood work to assess TSH and free T4 levels
Must first look for biological causes, a big one of which is hypothyroidism & |
|
|
TCAs, such as desipramine & nortryptilline, are
a.) not contraindicated in CAD, seizure disorder, BPH, dementia & constipation b.) to be avoided in the frankly suicidal, seeing as an overdose can kill c.) famous for causing significant orthostatic hypotension, weight gain and anticholinergic side effects, such as dry mouth & constipation d.) the one class of antidepressants that do not give sexual dysfunction e.) the first choice in the treatment of new onset depression in pregnancy |
b.) to be avoided in the frankly suicidal, seeing as an overdose can kill
|
|
|
One of your patient’s comes to you after the sudden death of her husband. He passed away 10 days ago after a massive MI, and she complains that she just cannot seem to feel better. She complains of depressed mood, insomnia, feeling worthless, anorexia (medically this means no appetite, do not confuse with anorexia nervosa, a control issue) & problems with agitation. You should:
a.) Reassure her that this is a normal part of bereavement. Ask about suicidal ideations, her support system, F/U if this does not pass. b.) Begin an SSRI. c.) Given her insomnia, consider trazadone therapy. d.) Refer her for grief counseling. |
a.) Reassure her that this is a normal part of bereavement. Ask about suicidal ideations, her support system, F/U if this does not pass.
Remember that to diagnose MDD, pt must have symptoms present for at least 2 weeks. Even if this had been going on for that long, it is important to realize that she has a clear inciting event to feeling sad. You must use your clinical judgment to decide if this woman is bereaving in a healthy fashion. Ask about suicidal thoughts and a support system. Also, remember that antidepressant agents take at least 6 weeks to give a full effect, so by the time they start to work, patient might be coming out of her mourning process. If patient insists on pharmacotherapy sedative, sometimes a sedative or a sleep aid to get them through this rough patch. |
|
|
Which of the following is not true regarding buproprion?
a.) it blocks the reuptake of DA b.) its metabolite blocks the reuptake of NE c.) it should not be given to patient’s with a history of seizure disorder d.) Best used as an adjuvant for MDD with insomnia, since it will cause sedation e.) Often used to help smokers quit smoking f.) May actually improve sexual function |
d.) Best used as an adjuvant for MDD with insomnia, since it will cause sedation
|
|
|
Which of the following is true regarding venlafaxine?
a.) NE reuptake inhibitor at lower dose b.) Should not be given in uncontrolled HTN c.) 5HT reuptake inhibitor at higher doses d.) It will not cause a serotonin withdrawal syndrome, the effects on NE counter such a reaction e.) It has numerous drug interactions, and can cause hepatic failure |
b.) Should not be given in uncontrolled HTN
|
|
|
MOA inhibitors work by
a.) Suppressing the enzyme that breaks down 5HT, NE, DA and tyrosine b.) Suppressing the reuptake of 5HT & NE only c.) blocking the 5HT2 & 5HT3 receptors, along with antagonizing presynaptic α2 receptors d.) inhibiting both MOA-A and MOA-B isoenzymes |
d.) inhibiting both MOA-A and MOA-B isoenzymes
|
|
|
Psychotherapy
a.) Shouldn’t be performed. Have you seeen One Flew Over the Cuckoo’s Nest?!? b.) Should be considered if a patient’s depression is refractory to treatment with at least two agents c.) Works by inducing a seizure, and could be harmful in pregnancy d.) Down regulates α-receptors to give a more rapid onset |
b.) Should be considered if a patient’s depression is refractory to treatment with at least two agents
|
|
|
Pick two of the substances that precipitate major side effects when given with phenelzine:
a.) the EtOH in wine, which could lead to a disulfram like reaction b.) the tyramine in EtOH and cheese, which could lead to a HTN crisis and consequential hemorrhagic stroke c.) lithium, which causes SIADH (syndrome of inappropriate ADH release) d.) opioids & sympathomimetics, which lead to a hyperexcitation syndrome, characterized by HTN, fever & delirium |
b.) the tyramine in EtOH and cheese, which could lead to a HTN crisis and consequential hemorrhagic stroke
d.) opioids & sympathomimetics, which lead to a hyperexcitation syndrome, characterized by HTN, fever & delirium |
|
|
EtOH and barbituates work by
a. Increasing the frequency of GABA channel openings b. Increasing the duration of GABA channel openings c. By blocking binding of a Cl channel d. Enhancing release and inhibiting the reuptake of DA & NE |
increasing the duration of GABA Ch opening
BZDs work on the same receptor as EtOH & barbs, but do so by increasing the frequency of GABA channel openings. All three thereafter work by binding to the GABA-A receptor and inducing a conformational change in the Cl channel, increasing the movement of Cl ions and thereby hyperpolarizing the neuron, making it unable to react to excitatory neurotransmitters. |
|
|
EtOH withdrawal is characterized by palpaltations, insomnia, delirium tremens, seizures and arrythmias. All of the following agents except which one is advised in the treatment of EtOH withdrawal
a. Benzodiazepines, like alprazolam b. Barbituates c. Phenytoin d. Β-blockers |
barbituates
Patients undergoing EtOH withdrawal should immediately begin therapy to decrease the two sequlae of withdrawal that can kill them, seizures & arrythmias. We give the phenytoin for seizure prophylaxis, and the beta-blockers for rate control. BZD treat the tremor and anxiety. Barbituates are an old school way of calming the nerves, but BZD are safer, we don’t see barbs used much anymore. |
|
|
Which of the following mechanisms explains the action of disulfram (antabuse) as a treatment for alchoholism after successful withdrawal?
a. Opioid antagonist that has been shown to reduce craving b. Unclear, possibly involving glutamate & GABA receptors c. Inhibition of aldehyde dehydrogenase, giving build up of acetaldehyde if patient consumes EtOH d. Inhibition of alcohol dehydrogenase, giving failure of EtOH metabolism |
c. Inhibition of aldehyde dehydrogenase, giving build up of acetaldehyde if patient consumes EtOH
|
|
|
EtOH gives increased estrogen to increase HDL, give gynecomastia and Dupytren’s contracture of the palm. It also increases gastric acid production, and suppresses appetite, accounting for a lot of the malnutrition that goes with alcoholism. It is contraindicated in pregnancy because it causes
a. Open neural tube defects b. Flattened face, joint defects, heart defects and mental retardation c. Malformed cartilage d. Kidney malformation, nervous system & cardiac anomalies |
b. Flattened face, joint defects, heart defects and mental retardation
What is described above is Fetal Alcohol Syndrome. Although a child may not have the facies or organ anomalies associated with intrauterine EtOH exposure, an isolated low IQ may be found. It is believed that FAS is more likely given the amount of exposure the child has to the drug, but there is no real cut-off where we see it. Many OBs allow a glass of wine a night, while still others feel safer encouraging complete abstinence from EtOH. Open neural tube defects are caused by folate deficiency, malformed cartilage comes with fluoroquinolones and effects under ‘d’ are attributed to many different drugs, including ACE-inhibitors. |
|
|
The craving, tolerance and dependence of chronic cocaine use can be explained by
a. A decrease in the amount of NE stored in neurons, seeing as it inhibited reuptake of NE for the duration of feeling high b. A decrease in the amount of 5HT stored in neurons, seeing as it inhbited reuptake of 5HT for the duration of feeling high c. A decrease in the amount of DA stored in neurons, seeing as it inhibited reuptake of DA for the duration of feeling high d. A decrease in the amount of DA stored in neurons, seeing as it inhibited reuptake of DA for the duration of feeling high. Also works as a direct agonists on the post-synaptic DA receptors. e. Enhanced release and inhibition of the reuptake of DA and NE, possible direct stimuation of α-receptors in the reward centers of the brain to give arousal, wakefulness & euphoria |
c. A decrease in the amount of DA stored in neurons, seeing as it inhibited reuptake of DA for the duration of feeling high
The exact MO of cocaine remains a mystery, but this is what we think at this point. |
|
|
Amphetamine and related stimulants are used medically in the treatment of
a. Depression, to give patients the urgent stimulation needed to rescue them from suicidal ideations b. ADHD, paradoxically stimulating to pay attention. c. Never, these compounds are derived into methamphetamine, a terrible drug with high dependence rates d. Insomnia, paradoxically focuses the mind enough to defer racing thoughts that may contribute to an inability to go to sleep |
ADHD paradoxically stimulating to pay attention
Other uses of stimulants include modafanil for narcolepsy & ephedrine for weight loss, although the latter is banned by the FDA. What makes meth much worse than the other amphetamines is the fact that it is resistant to metabolism by MAO, keeping it around a lot longer. |
|
|
The DA theory of psychosis is explained by all except the following
a. DA blocking medications have antipsychotic effects b. DA agonists may cause psychosis c. Increased density of DA receptors in the brains of the psychotic d. Propsychotic effects of amphetamines known to cause central DA release. e. Atypicals having a high affinity for D2 |
atypicals having a high affinity for D2
Typicals have a high affinity for D2. Atypicals actually have a low affinity for D2, making them less apt to cause EPS. This truth is actually one of the barriers for DA as a solitary explanation of psychosis. |
|
|
One of the main drawbacks in using typical antipsychotics in the treatment of psychosis is
a. They act also as Ach agonists, giving sweating, N/V/D and urinary incontinence b. Neuroepileptic malignant syndrome c. They activate α receptors, making them a huge problem to patients with BPH d. They act as a histamine receptor agonists, causing the flushing and itchiness seen with other drugs that act on histamine, like vancomycin & morphine e. Resolution of the negative symptoms, with little effect on the positive symptoms, leaving patients with delusions and hallucinations |
neuroepileptic malignant syndrome -- FATAL!!
|
|
|
9.) The negative symptoms of psychosis can be more destructive than positive symptoms in many respects, and the patient’s personality never returns to baseline after a bout of negative symptoms. They can be remembered as the 5 A’s, including all but which of the following?
a. Avolition (lack of desire, motivation to pursue goals) b. Anhedonia (no pleasure in fun activities) c. Anabolic behavior d. Asocial e. Affect blunting f. Alogia (without speech) |
anaboloic behavior
People with schizophrenia do not build big molecules from small molecules. But they do often enter into a catatonic state, which is not a catabolic state, but rather means loss of motor skills. |
|
|
The atypical antipsychotics have less EPS and endocrine dysfunction than the typicals, work on both the positive & negative symptoms of schizophrenia and all could be used as mood stabilizers in bipolar disorder as well. Their MO is
a. High affinity block of D2 with antagonism of histamine, alpha, and cholinergic receptors. b. Low affinity block of D2 to decrease EPS, with concurrent block of 5HT2A to cause a reduction in prolactin release. c. Inhibit the release of DA & NE, increase release of 5HT & enhance GABA d. Inhibit reuptake of DA & NE e. Inhibit reuptake of 5HT & NE |
b. Low affinity block of D2 to decrease EPS, with concurrent block of 5HT2A to cause a reduction in prolactin release.
Typicals have a high affinity block of D2, making them very good at eliminating the hallucinations and delusions of psychosis, but also increasing their likelihood of causing EPS. Li works to inhibit release of DA & NE, increase 5HT and enhance GABA. The reuptake of DA and NE is how buproprion works, so you could imagine this would be the wrong drug to give to someone who is bipolar, you would most certainly shoot them into a manic phase. The reuptake of 5HT and NE is prevented by the TCAs, like nortryptilline. |
|
|
Risperidone is an atypical that acts the most like a typical when given in high enough doses. The most effective of the atypicals is clozapine, because it works on positive, negative and suicidality. Which of the following is not an adverse effect of clozapine?
a. Sedation b. Seizures c. Respiratory depression d. Agranulocytosis e. Weight gain, DM II, dyslipidemia |
respiratory depression
Clozapine is the most dangerous of the atypicals, in addition to being the most effective. The rate of agranulocytosis is about 2%, which could give dangerous infection. Also, seizure rate is as high as 4%. The sedation, along with bed wetting and orthostatic hypotension are part of the anticholinergic effects that come along with most of the atypicals. Remember that almost all the atypicals can cause metabolic syndrome, some more than others. |
|
|
Mania can be defined as >1 wk of inflated self-esteem, decreased need for sleep, racing thoughts and involvement of pleasurable activities. If these behaviors were extreme enough to require hospitalization, they do not need to have occurred for at least a week to be defined as a mania. Acute mania of bipolar is best managed by
a. Li with lamotrigine b. Valproate, with a barbiturate to tide the patient over c. Li alone d. Li with a barbiturate to tide the patient over e. Li with a BZD or antipsychotic to tide the patient over |
e. Li with a BZD or antipsychotic to tide the patient over
Li is the gold standard in the tx of bipolar and should be first line. It is slightly better working on the mania than the depression of bipolar, but still, first line. If that does not work, we could move to valproate. To really break a manic episode though, neither of these would be effective, and patients need to be acutely managed with a BZD or antipsychotic. |
|
|
Adverse effects of Li occur up to 75% of the time, and this really limits patient compliance. These include which of the following?
a. Nephrogenic diabetes insipidus b. Central diabetes insipidus c. SIADH d. Hyperthyroidism e. Hypothyroidism f. Rash g. Tremor h. N/V/D i. Weight gain j. Impotence k. Acne l. Pulmonary fibrosis |
nephrogenic DI
hypothyroidism rash tremor NVD weight gain acne Li does a lot. You want to treat the tremor with a beta-blocker and treat the nephrogenic DI with a thiazide diuretic. Remember that like most of the drugs used to treat bipolar, Li is REALLY teratogenic, causing floppy baby, cardiac malformation and cretinism. This is why electroconvulsive therapy is the treatment of choice in pregnant bipolar patients. |
|
|
Which of the following is false regarding lamotrigine?
a. Takes up to 2 mos to work b. Blocks Na channels & increases both aspartate & glutamate c. Is often more effective for the depression of bipolar than even lithium d. If used with Li, the dose of lamotrigine should be halved |
If used with Li, the dose of lamotrigine should be halved
If lamotrigine is given with valproate, the dose of lamotrigine should be halved. |
|
|
Bipolar disorder has many variations, one of which is termed rapid cycling. Rapid cyclers experience at least 4 major manic and/or depressive episodes in 12 mos time. Although Li has been shown to temper mania, reduce depression and decrease suicidality, rapid cyclers are sometimes better managed with
a. Lamotrigine b. Carbamazepine c. Oxcarbazepine d. Fluoxetine e. clonazepam f. valproate |
valproate
Even though lamotrigine might do better on the depression of bipolar disorder, this is practically the only time where you would consider using anything but Li first line, in terms of effectiveness. In the real world, we see a lot of atypical antipsychotics used as monotherapy in the treatment of bipolar disorder. |
|
|
Parkinson’s Disease is characterized by all of the following cardinal symptoms except:
a. Resting tremor b. Posture and gait abnormalities c. Cogwheel rigidity d. Lead pipe rigidity e. Akinesia & bradykinesia |
lead pipe rigidity
When thinking PD, think T.R.A.P - - > 1.) tremor (resting). Intention tremor indicated cerebellar damage, essential tremor is benign & famously relieved by EtOH; 2.) rigidity (cogwheel). Lead pipe rigidity indicates UMN damage. 3.) Akinesia & bradykinesia 4.) postural stooping & ataxia. |
|
|
Dopamine agonists are often used in younger patients, before the initiation of LD/CD, and as adjuvants to LD/CD in the treatment of dyskinesias. Adverse effects of DA agonists include:
a. Impulse control disorders, manifest by pathologic gambling, excessive shopping, binge eating or hypersexuality b. Insomnia c. Extreme nausea and vomiting, enough so to be taken with trimethobenzamine d. Fatal hepatotoxicity e. Dry mouth, constipation, urinary retention and aggravation of glaucoma |
a. Impulse control disorders, manifest by pathologic gambling, excessive shopping, binge eating or hypersexuality
Extreme nausea and vomiting is an adverse effect of apomorphine, while fatal hepatotoxicity is something we worry about with the COMT inhibitors entacapone and tolcapone, and the anticholinergic effects are caused by trihexyphenidyl and benztropine. |
|
|
Levodopa/Carbidopa can be administered as a controlled release formulation, controlled release + immediate release, liquid levodopa and as an orally dissolving tablet commercially available. The CR formulations have which of the following advantages (2)
a. Fewer daily doses b. More reliable absorption c. A measurable effect on freezing & other motor complications d. Less plasma fluctuations e. Can be used as a rescue medication during ‘off’ episodes |
fewer daily dose, less plasma fluctuations
LD/CD is famously erratically absorbed, complicated by eating lots of protein, and this is made only worse by the CR formulation. Remember that in general, LD/CD treats the bradykinesia pretty well, but does not do too much for the tremor, and does not have a measureable effect on the ‘freezing’ that occurs later on in the disease. And although the ‘liquid levodopa’ formulation can be used as a rescue med for an ‘off’ attack, the CR formulation is dissolved way too slowly to have such an acute indication. |
|
|
Levodopa is a precursor to DA. Adverse effects include all of the following except:
a. N/V, anorexia b. Orthostatic hypotension c. Urinary retention d. Vivid dreams, hallucinations and sleep attacks, most severe in the elderly with dementia |
urinary retention
Urinary retention may be an adverse effect of an anticholinergic, but all of the other effects listed above are due to levodopa. The anorexia & N/V, along with the orthostatic hypotension, both get better with continued treatment. |
|
|
LD/CD is the gold standard in the treatment of Parkinson’s disease. Limitation to its long-term use is due to
a. Likely chance of hepatotoxicity after about 8 years b. Development of neuroleptic malignant syndrome after about 8 years c. Failure of oral absorption makes the drug only available IV, and veins cannot sustain this for more than about 8 years d. Vivid dreams, hallucinations and sleep attacks, which are refractory to antipsychotic management, and eventually account for the dementia of this condition e. Narrowing of the therapeutic window, giving patients both increased dyskinesias and failure of the ‘off’ response |
e. Narrowing of the therapeutic window, giving patients both increased dyskinesias and failure of the ‘off’ response
8 years is about the maximum amount of time we expect LD/CD to work. Yet, it will not cause hepatotoxicity (that is your COMTs, your ‘capones’, think capone drank lots of booze and his liver pooped out). Neuroleptic malignant syndrome is caused by antipsychotics, drugs that are essentially the opposite to our PD drugs. The vivid dreams happen, but they do not account for the psychosis, nor are they usually enough of a contraindication to D/C the best drug we have for PD. |
|
|
Benzodiazepines are used in the treatment of acute anxiety and often as a sleep aid. Their mechanism of action is
a. Decreasing DA release b. Inhibiting the reuptake of DA, 5HT, NE & tyramine c. Increasing the frequency of opening of Cl channel on GABA receptors d. Increasing the duration of opening of Cl channel on GABA receptors e. Decreasing the reuptake of GABA in the brain |
c. Increasing the frequency of opening of Cl channel on GABA receptors
Remember that BZD (benzodiazepenes) work on the same channel as barbituates and EtOH. BZDs open the channel more frequently, while EtOH and barbs keep the channel open longer. Either way, GABA agonists increase Cl conductance to hyperpolarizes neuronal membranes and counter the effect of excitatory neurotransmitters. This is why taking these drugs together is an absolute CI. |
|
|
All of the following are true regarding zolpidem except:
a. At therapeutic concentrations, it binds to the α1 receptor, thereby minimizing the anxiolytic effect that would be had by binding the α2 receptor and the sensory changes that come with binding the α3 receptor b. Minimal dependence potential c. Not indicated as an anticonvulsant or a muscle relaxant d. No effect on REM sleep e. Decreases the quality of slow wave sleep |
decrease the quality of slow wave sleep
Zolpidem and the other non-BZD, zaleplon & zipiclone, increase the quality of slow wave sleep. This is why people do crazy sleep walking things on Ambien. |
|
|
Other drugs used in the management of insomnia include
a. OTC antihistamines b. Pain relievers that include codeine c. Sedating antidepressants like buproprion d. Melatonin receptor antagonists like ramelteon e. Fluamzenil |
OTC antiHistamines
OTC with antihistamines are famous for causing drowsiness, even though there are better options out there. Although codeine containing analgesics do make you drowsy, their main indications are as an antitussive & analgesic. Buproprion is not a sedating antidepressant, but the exact opposite, keeping DA & NE around longer, helping people quit smoking and keeping people awake. Trazadone on the other hand is a sedating antidepressant. Ramelteon is a melatonin receptor agonist, not antagonist. Flumazenil is a red herring, and has nothing to do with sleep, but is rather an antidote to BZD OD. |
|
|
Flurazepam and quazepam are rapid onset, long acting BZD. With administration of these agents, we worry about all of the following except
a. Daytime sedation b. Rebound insomnia c. A withdrawal syndrome, that includes insomnia, photophobia, tinnitus and seizures. d. Patient’s concominant use of EtOH and barbituates |
rebound insomnia
Rebound insomnia is unlikely to occur in a patient taking a long acting BZD since there is less of a crash. But, daytime sedation is more likely to occur with an aget like flurazepam or quazepam then something like triazolam, a short acting which is good at putting you to sleep rather than keeping you that way through the night (triazolam = tri to go to sleep). The withdrawal syndrome and use of EtOH and barbs is something we worry about with all BZD. |
|
|
dyskinesias:
a) Levodopa/Carbadopa b) amatadine c) benztropine d) apomorphine |
amantadine
|
|
|
tremor and drooling
a) Levodopa/Carbadopa b) amatadine c) benztropine d) apomorphine |
benztropine
|
|
|
What meds can help with hallucinations that cause problems
a) Levodopa/Carbadopa b) amatadine c) benztropine d) apomorphine e) quetiapine |
quetapine atypical anitpsychotic
|
|
|
"on-off' phenomenon
a) Levodopa/Carbadopa b) amatadine c) benztropine d) apomorphine |
apomorphine
|
|
|
best drug fo PD:
a) Levodopa/Carbadopa b) amatadine c) benztropine d) apomorphine |
Levodopa/Carbadopa
|
