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CNS > Exam 3 Practice Questions > Flashcards

Exam 3 Practice Questions Flashcards

1
Q
  1. What is happening physiologically to cause loss of movement in Parkinson’s disease (PD)?
    a. Loss Ach in the substantia nigra
    b. Loss of DA in the substantia nigra
    c. Loss of 5 HT in the raphe
    d. Loss of Ach in the VTA
A

b. Loss of DA in the substantia nigra

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2
Q
  1. True or False: DA metabolites can cause PD
A

True

Answer: Due to the oxidative damage done on DA neurons causing cell death

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3
Q
  1. What are the hallmark sx of PD? Select all
    a. Difficulty swallowing
    b. Bradykinesia
    c. Muscle rigidity
    d. Weight loss
    e. Resting tremor
    f. micrographia
    g. Postural instability
    h. Quiet speech
    i. Constipation
A

b. Bradykinesia
c. Muscle rigidity
e. Resting tremor
g. Postural instability

Answer: the others are just other sx of PD

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4
Q
  1. What is the basal ganglia’s output to the thalamus?
    a. Striatum Caudate
    b. Substantia nigra
    c. Globus Pallidus GPi
    d. Motor cortex
    e. Globus Pallidus GPe
A

c. Globus Pallidus GPi

Answer: it goes from SN -> striatum -> basal ganglia GPi -> Thalamus -> cortex -> movement. It’s also in her picture she gave. She also mentioned just the globus pallidus, so unsure of if you need to know if it is GPi or not but decided I should mention it

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5
Q
  1. True or False: The d2 receptor pathway has a direct beneficial effect on treating PD.
A

False.

Answer: It has an indirect pathway and it gives more advantages to treating PD than D1

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6
Q
  1. If we want there to be movement, which of these has to occur?
    a. Inhibition of the thalamus
    b. A gabaergic signal output from the basal ganglia
    c. A gabaergic signal output to the basal ganglia from the striatum
    d. A glutaminergic signal output to the basal ganglia
A

c. A gabaergic signal output to the basal ganglia from the striatum
Answer: A B and D are the same thing in a sense. A gabaergic signal form the basal ganglia will inhibit the thalamus causing there to be no movement (no glutaminergic output from thalamus). If we have a glutaminergic signal to the basal ganglia then that is activating to allow for a gabaergic signal to the thalamus, inhibiting it. If we had a gabaergic output then it would inhibit the basal ganglia and allow the thalamus to send signals to the motor cortex.

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7
Q
  1. What are the parts of the basal ganglia?
A

Striatum (caudate, putamen), Globus pallidus (GPe, GPi), Substantia nigra (SNc, SNr), subthalamic nucleus

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8
Q
  1. What is the use of adding Carbidopa in conjunction with L-DOPA
    a. It works in an additive way with DA to help reduce PD by acting in the brain
    b. It increases DA in the periphery and the brain to allow for better drug therapy
    c. It is a DA agonist which would help the sx
    d. It inhibits AADC which prevents breakdown of L-dopa in the periphery and allows it to enter the BBB
A

d. It inhibits AADC which prevents breakdown of L-dopa in the periphery and allows it to enter the BBB
Answer: It doesn’t cross the BBB so it will allow for L-dopa to be converted there. AADC is the enzyme that converts L-dopa to DA and it prevents DA conversion in the periphery

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9
Q
  1. Which COMT inhibitor has both a central and peripheral effect?
    a. Entacapone
    b. Tolcapone
    c. Selegiline
    d. Carbidopa
A

b. Tolcapone

Answer: it isn’t used as often due to it’s hepatotoxicity and but entacapone doesn’t cross the BBB so MAOis might be more useful to inhibit DA degradation in the brain

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10
Q
  1. Which of these is a NOT an advantage of DA agonists
    a. Don’t need conversion
    b. No free radical metabolites with the DA agonist metabolites
    c. Not active in normal release characteristics
    d. There can be specificity for the DA receptor subtypes
A

c. Not active in normal release characteristics

Answer: it doesn’t have the same release as DA which releases at the right time to initiate the movement circuit;

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11
Q
  1. Bromocriptine and Apomorphine both have activity at the D1R and D2R but apomorphine is not considered an ergot alkaloid DA agonist because
    a. It doesn’t cause the same ADRs as bromocriptine
    b. It is a full agonist at d1R while bromocriptine is a partial agonist
    c. It is specific for D2Rs
    d. It’s administered SC
A

a. It doesn’t cause the same ADRs as bromocriptine

Answer: bromocriptine causes the ergotism vasoconstriction in the periphery while apomorphine does not

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12
Q
  1. Assign the numbers to the metabolism: choices are MAO, COMT, Aldehyde dehydrogenase (AD)
A
  1. COMT 2. MAO 3. MAO 4. COMT 5. AD 6. AD 7. COMT
    Answer: major urinary metabolite is HVA which undergoes all of those. Minor is DOPAC which doesn’t go through COMT metabolism. The other two are to get to NE (DABH) and Epi (DABH then PENT)
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13
Q
  1. Which of these DA agonist undergoes O glucoronidation and sulfation AND has a patch formulation
    a. Neupro
    b. Apokyn
    c. Mirapex
    d. Requip
A

a. Neupro

Answer: can be neuroprotective in the sense that it doesn’t form oxidative metabolites and DA is being taken out of the picture (not enough evidence); n-depropylation and then conjugation can occur first; main conjugation is sulfation

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14
Q

Which of these drugs can be metabolized by CYP1a2?

a. Selegiline
b. Neupro
c. Stalevo
d. Rasagiline

A

d. Rasagiline

Answer: may be neuroprotective as well due to the slow metabolism of DA to toxic metabolites

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15
Q
  1. Amantadine enters the BBB due to:
    a. It is unionized and lipophilic
    b. It’s structure is caged like so it is able to enter the BBB
    c. It has low pKa that allows it go into the BBB
    d. It has a transporter
A

b. It’s structure is caged like so it is able to enter the BBB

Answer: it is ionized due to a pKa of 11 but bc of it’s structure it is lipophilic enough to go in

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16
Q
  1. JK is a 57 YOF presenting with a pill rolling motion in her hands that don’t bother her while sleeping and rigidity in her arms. She denies taking any medications at the moment. What diagnostic criteria do you place her in?
    a. Clinically probable for PD
    b. Clinically definite for PD
    c. Clinically possible for PD
    d. Clinically possible for EPS
A

a. Clinically probable for PD

Answer: JK is presenting with 2 of the 3 cardinal diagnostic sx of PD without pharmacotherapy. If she was presenting with 3 of the cardinal sx without pharmacotherapy she would still be clinically possible

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17
Q
  1. Which drug causes the most motor complications such as dyskinesias?

a. Comtan
b. Symmetrel
c. Congentin
d. Sinemet

A

d. Sinemet

Answer: That is L-Dopa and carbidopa; levodopa causes the most motor complications

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18
Q
  1. In younger patients, why isn’t L-Dopa considered first line? Select all
    a. Want to save the best for last
    b. It is the worst agent to use for symptom control
    c. It has increased motor complications in long term patients
    d. It is not as effective as an MAO B inhibitor
    e. It is the gold standard
    f. It is not as effective as amantadine
A

a. Want to save the best for last
c. It has increased motor complications in long term patients
Answer: in older pts (>65) it is first line; due to dyskinesias with long term use we want to reserve it for later and to avoid a subtherapeutic effect with long term use; it is the best for symptom control action. MAO B inhibitor is the first line but not better than L-Dopa. It is the gold standard but that is not why it isn’t first line

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19
Q
  1. Which of these is a rescue treatment for the freezing that often occurs in advanced PD?
    a. Pardolel
    b. Neupro
    c. Requip
    d. Mirapex
    e. Apokyn
A

e. Apokyn

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20
Q
  1. True or False. Cholinergic neurons are the only neurons that are affected in Alzeimer’s disease.
A

False.

Answer: they are just the most vulnerable and likely, not the only ones

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21
Q
  1. Which of the following is not a risk factor for developing alzeimer’s?
    a. Down Syndrome
    b. Intake of omega 3 fatty acids
    c. Hypertension
    d. High insulin use
    e. Low education level/IQ
    f. Hypercholesteremia
A

b. Intake of omega 3 fatty acids

Answer: may help actually along with Vit C,D, and E, but it isn’t proven

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22
Q
  1. Which of these drugs is not a cholinesterase inhibitor?
    a. Aricept
    b. Exelon
    c. Razadyne
    d. Namenda
A

d. Namenda

Answer: It is NMDA antagonist that blocks the leaky glutamate channels causing exocitotoxicity. It can be overcome by normal glutamate function

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23
Q
  1. Which drug has pseduoirreversibility due to its carbamate functional group?
    a. Tacrine
    b. Donezepil
    c. Rivastigmine
    d. galantamine
A

c. Rivastigmine

answer: the carbamylation of rivastigmine causes slow hydrolysis of the bound AchE which lasts 10 hours

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24
Q

Match the numbers with the metabolism. For #5 name the active metabolite. N-dealkylation, FMO facilitated N-oxidation, O-demethylation, aromatic hydroxylation

A
  1. O-demethylation
  2. N-dealkylation
  3. FMO facilitated N-oxidation
  4. Aromatic hydroxylation
  5. 1 (O-demethylation)
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25
Q
  1. Match the disorder with the characteristic
    a. Old age i. significant cognitive impairment
    b. Mild neurocognitive disorder ii. Decline in memory, small hippocampi
    c. Major neurocognitive disorder iii. Absence of effects on ADLs
    d. Alzeimer’s disease iv sudden onset, cortical/subcortical changes on MRI
    e. Vascular dementia v. Visual hallucinations, parkinsonism
    f. Lewy body dementia vi modest cognitive impairment
    g. Frontotemporal dementia vii. Effects seen with L-DA
    h. Parkinson’s dementia viii disinhibtion, atrophy in frontal, temporal lobes
A

a. iii
b. vi.
c. i.
d. ii
e. iv
f. v
g. viii
h. viii

26
Q
  1. Which of these is indicated to treat at all stages of alzeimers (mild-severe)?
    a. Tacrine
    b. Aricept
    c. Razadyne
    d. Exelon
    e. Namenda
A

b. Aricept

Answer: Namenda can be used in moderate-severe alzeimer’s but not indicated in mild

27
Q
  1. Which of these can be used to treat dementia associated with Parkinson’s and Alzheimers?
    a. Tacrine
    b. Aricept
    c. Razadyne
    d. Exelon
    e. Namenda
A

d. Exelon

28
Q
  1. JK has been diagnosed with mild Alzheimer’s disease. What is the appropriate treatment plan to start him on?
    a. Namenda
    b. Donepezil 5 mg
    c. Donepezil 10 mg
    d. Donepezil 23 mg
A

b. Donepezil 5 mg

Answer: must titrate it up and initial dosing is 5 mg, only severe patients get 23 mg and only mod-severe patients get Namenda

29
Q
  1. JK has been diagnosed with mild Alzheimer’s disease and started on donepezil. What counseling should we give to JK about their donepezil? Select all
    a. Can raise your blood pressure
    b. Do not crush or split the tablet
    c. You may see brownish urine
    d. Anorexia and weight loss
    e. Syncope or bradycardia can occur
A

b. Do not crush or split the tablet
d. Anorexia and weight loss
e. Syncope or bradycardia can occur

Answer: it lowers the blood pressure, also it causes SLUDE effects

30
Q
  1. JK was started on the Exelon patch 2 months ago and was at a dose of 9.5 mg/24 hours. He became sick 5 days ago and had NVD. He feels better now but hadn’t been taking his patch for those 5 days. How should the treatment be changed?
    a. Decrease the dose to 4.6 mg/day patch
    b. Keep him at the same dose
    c. Switch him to the oral dosing form at 6 mg BID
    d. Recommend that he wait a few more days and then start the 9.5 mg/24 hours dose again
A

a. Decrease the dose to 4.6 mg/day patch

Answer: if it’s been >3 days reinitiate at lowest starting dose; if

31
Q
  1. Which of these can be used in vascular dementia?
    a. Aricept
    b. Razadyne
    c. Exelon
    d. Namenda
A

d. Namenda

Answer: although it is not statistically significant, it is still used in vascular dementia (she recommended it under her recommendations)

32
Q
  1. Desensitization is associated with all of these except:
    a. G-protein undocking to where there is no response when the agonist binds the receptor
    b. G-protein being activated and activating second messengers
    c. Internalization of the mu opioid receptors
    d. Tolerance can occur with long term desensitization
A

b. G-protein being activated and activating second messengers

Answer: that is the normal function of the g-protein receptor without desensitization

33
Q
  1. Mu opioid agonism on the periaqueductal gray results in: (select all)
    a. Increases release of 5HT and NE
    b. Increased release of GABA
    c. Disinhibition of the medullary neurons
    d. Alpha 2 antagonism
    e. Inhibition of glutamate receptors on interneurons
A

a. Increases release of 5HT and NE
c. Disinhibition of the medullary neurons

Answer: it blocks gabaergic interneurons from releasing gaba onto medullary neurons. This allows the medullary neurons to ultimately increase releas of 5ht and NE that will give a better feeling of euphoria and antidepression

34
Q
  1. Which of these receptors when agonized has the effect of sedation, constipation, analgesia, respiratory depression, and reward?
    a. Mu
    b. Kappa
    c. Gamma
    d. Lamda
    e. Delta
A

a. Mu

35
Q
  1. Aversion is an effect of the agonism of which of these opioid receptors?
    a. Mu
    b. Kappa
    c. Gamma
    d. Lamda
    e. Delta
A

b. Kappa

Answer: dynorphins are endogenous ligand that cause a dissociative feeling

36
Q
  1. Which of these is involved in you localizing the pain you are feeling (e.g feeling the pain in your right hand after hitting it in your car door)?
    a. Thalamus (thalamic tract)
    b. Hippocampus (hippocampic tract)
    c. Brainstem (reticular tract)
    d. Periaqueductal gray
A

a. Thalamus (thalamic tract)
Answer: thalamus sends the signal back to the origin of the stimulus to make you feel a sense of pain; it is somatotopically organized (every time you stick that neuron in the brain you will feel pain in that same spot – the right hand); PAG is involved in your body’s response to the pain-such as endogenous opioid release (endorphins)

37
Q
  1. Which of these is involved in you feeling the emotion of pain and understanding what just happened?
    a. Thalamus (thalamic tract)
    b. Hippocampus (hippocampic tract)
    c. Brainstem (reticular tract)
    d. Periaqueductal gray
A

c. Brainstem (reticular tract)

Answer: the brainstem gives you the awareness of pain; may carry some intensity but has zero localizaton

38
Q
  1. How does clonidine, gabapentin, and pregabalin help in neuropathic pain?
    a. They are Gaba A antagonists
    b. They are alpha 2 agonists
    c. They are effective in 5ht and NE release to help stop excitation of glutamate receptors
    d. They decrease activity in the calcium ion channel, decreasing inappropriate excitation and propagation in neuropathic pain
A

d. They decrease activity in the calcium ion channel, decreasing inappropriate excitation and propagation in neuropathic pain
Answer: they have different mechanisms of action but this is the gist of what both of them do in neuropathic pain; pregabalin and gabapentin block the calcium channel and clonidine decreases activity in the calcium ion channel according to Sharpe

39
Q
  1. Which fibers are only activated when there is a noxious stimuli that crosses a high threshold (in a normal patient)
    a. A beta fibers
    b. A delta fibers
    c. C fibers
    d. A gamma fibers
A

c. C fibers

Answer: C fibers relay information about severe pain; like extreme pain. A delta fibers would be relayed first since they are faster; but C fibers would have to have a severe stimulus to be activated even. A beta is for non-noxious stimuli and it is the fastest out of all of them but it only receives non-noxious stimuli

40
Q
  1. What is true about chronic pain? Select all
    a. It could be due to increased sensitivity of the first order neurons which increases glutamate release onto second order neurons
    b. It could be due to increased sensitivity of the first order neurons which increases GABA release onto second order neurons
    c. It could be due to increased insensitivity of the second order neurons which receives glutamate and doesn’t send a signal to the brain
    d. It could be due to increased sensitivity of the second order neurons that receives a normal release of glutamate and sends a message of extreme pain to the brain when there is not truly harmful stimuli
A

a. It could be due to increased sensitivity of the first order neurons which increases glutamate release onto second order neurons
d. It could be due to increased sensitivity of the second order neurons that receives a normal release of glutamate and sends a message of extreme pain to the brain when there is not truly harmful stimuli

41
Q
  1. Which of these mixed agonists for pain is a Kappa antagonist?
    a. Nubain
    b. Stadol
    c. Suboxone
    d. Talwin
A

c. Suboxone

Answer: buprenorphine is a Kappa antagonist and mu partial agonist; the rest are Kappa agonists and mu partial agonist/antagonist

42
Q
  1. If you are a ____ poor metabolizer, you would not be able to feel the analgesic effects of codeine because it will not be metabolized into morphine.
    a. 2d6
    b. 3a4
    c. 2c19
    d. Phase II
A

a. 2d6

43
Q
  1. Which of the following is true about hydrocodone’s 3-OCH3 methyl? Select all
    a. It decreases entry into the brain
    b. It increases lipophilicity
    c. It causes hydrocodone to be more potent than morphine
    d. It decreases the affinity for the mu receptor activity, lowering the effectiveness
    e. It decreases its antitussive effects
A

b. It increases lipophilicity
d. It decreases the affinity for the mu receptor activity, lowering the effectiveness

Answer: it increase entry into the brain due to lipophilicity, and it is less potent than morphine bc of the decreased affinity on the mu receptor

44
Q
  1. Which of the following is not true about phenanthrenes?
    a. If R1 is a 3 carbon chain or longer, the molecule most likely has antagonist activity
    b. R2 can be an OH or H
    c. R3 can be an OH or H
    d. If R4 does not have an OH group, it has increased lipophilicity
    e. The levo isomer is the active molecule
A

b. R2 can be an OH or H

Answer: R2 must have OH for mu or K receptor activity

45
Q
  1. Which of these additions would cause the drug to have greater antitussive activity and may lose some of its analgesic activity?

a. Hydrolysis of alkene on C7-C8
b. Methylation of 3-OH
c. 3 carbon chain on tertiary amine
d. OH addition on C-14

A

b. Methylation of 3-OH
Answer: codeine, dextromethorphan, and hydrocodone/oxycodone have this addition which increases the antitussive activity and seem to have lowered analgesic activity when this is added. This just a pattern I saw in his notes and seemed like a question he might ask. According to Frei, there isn’t much antitussive effect with hydrocodone though.

46
Q

Which is not true about Alvimopan?

a. It is a zwitterion
b. It crosses the BBB
c. It relieves the peripheral ADRs of opiates
d. It is a peripherally acting mu opioid receptor antagonist
e. It stays in the gut because it cannot cross lipid membranes

A

b. It crosses the BBB

Answer: it is PAMOR so it doesn’t cross BBB

47
Q
  1. JK has been classified into Step 2 of the WHO with a rating of 5 on the pain scale. She has never taken any opioids before and doesn’t have any renal or liver failure. What drug is appropriate for her?

a. Tramadol
b. Morphine
c. Fentanyl
d. Ibuprofen

A

a. Tramadol

Answer: step 1 (1-3) is D, Step 2 (4-7)- weak opioids; step 3 (8-10) B and C are in step 3

48
Q
  1. If a patient is receiving a dose of 100 mg BID of MS contin, what should their breakthrough medication be?
    a. Hydrocodone 10 mg/325 mg q 4 hours
    b. MS immediate release 20 mg q 2 hours
    c. MS contin ER 100 mg q 4 hours
    d. MS immediate release 10 mg q 2 hours
A

b. MS immediate release 20 mg q 2 hours

Answer: should be 10-20% of the total daily dose

49
Q
  1. Match dosing interval with the drug. May be used more than once and can use a time within a range
    a. Morphine CR i. 8 hours
    b. Morphine IR ii. 12 hours
    c. Codeine iii 6 hours
    d. Hydrocodone/APAP iv 72 hours
    e. Hydrocodone v 4 hours
    f. Oxycodone CR vi. 2 hours
    g. Oxycodone IR
    h. Methadone
    i. Fentanyl
    j. Tramadol
A 
Answer: 
a 12 hours 
b 2 hours 
c 4 hours 
d 4-8 hours 
e 8 hours 
f 8 hours 
g 6 hours 
h 8 hours 
i 72 hours 
j 8 hours
50
Q
  1. For what indication can you use Demerol for?
    a. Analgesia
    b. Rigors
    c. Cough
    d. Pulmonary edema
A

b. Rigors

Answers: because Toxic metabolites accumulate with repeated dosing, Associated with seizures, and Renal insufficiency

51
Q

Which of these is more likely to cause pruritis in a patient? Select all

a. Hydrocodone
b. Oxycodone
c. Codeine
d. Methadone
e. Morphine

A

c. Codeine
e. Morphine

Answer: due to high histamine release; these are the highest releasers of it; along with meperidine

52
Q
  1. True or False.
    A stool softener alone is first line for constipation in patients taking opioids. A laxative stimulant can be added later if it is not working.
A

False.

Answer: must have both a stool softener and laxative stimulant

53
Q
  1. Match the drug interaction with the effect
  2. CNS depressants, SJW, alcohol
  3. TCA
  4. Erythromycin
  5. Methadone/Morphine
  6. 2d6 inhibitors
  7. Quinine
  8. Rifampin
  9. 2d6 substrates
  10. Metoclopramide
  11. Meperidine/Tapentadol
A

Answers:

  1. j
  2. a
  3. f
  4. b
  5. h
  6. c
  7. g
  8. d
  9. i
  10. e
54
Q
  1. Which of these drugs can cause QTc prolongation
    a. Morphine
    b. Methadone
    c. Hydrocodone
    d. Fentanyl
A

b. Methadone

Answer: it has a BBW

55
Q
  1. What can increase delivery of fentanyl into the body? Select all
    a. Decreased fat
    b. Cold showers
    c. Hot showers
    d. Hairy area for placement
    e. Fever
    f. Broken skin
A

c. Hot showers

e. Fever
f. Broken skin

Answer: the others decrease delivery

56
Q
  1. True or false.

You have to be physically dependent on a drug to be addicted

A

False.

Answer: addiction can occur without dependence (dependance is classified by withdrawal on cessation)

57
Q
  1. What is the initial dosing for gabapentin in diabetic neuropathy?
    a. 300 mg TID
    b. 100 mg TID
    c. 900 mg daily
    d. 100 mg daily
A

b. 100 mg TID

answer: it needs to be tirated up; the effective dose is 900-3600 mg/day TID dosing

58
Q
  1. What is the max dose of Lyrica in diabetic neuropathy?
    a. 100 mg daily
    b. 100 mg TID
    c. 900 mg daily
    d. 200 mg TID
A

b. 100 mg TID

answer: max dose is 300 mg/day; in postherpetic neuropathy it is 600 mg/day

59
Q
  1. Which drug autoinduces cyp450 enzymes
    a. OXC
    b. Tramadol
    c. Pregabalin
    d. CBZ
A

d. CBZ

60
Q
  1. Which drugs should be avoided in seizures: select all
    a. Tramadol
    b. CBZ
    c. Pregabalin
    d. TCAs
    e. Tapentadol
A

a. Tramadol

e. Tapentadol

CNS (7 decks)

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