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BCN EXAM 5 > Neurotoxic drugs > Flashcards

Neurotoxic drugs Flashcards

1
Q

Dopaminergic treatment of parkinson’s disease could lead to

A

Hallucinations, paranoia

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2
Q

Neuroleptic treatment of schizophrenic and psychosis

A

drug induced parkinsonism

dopaminergic

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3
Q

AchE inhibitor drug treatment for Alzheimer could lead to

A

Tremor

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4
Q

Anti-Ach drug treatment for parkinson’s disease could lead to

A

confusion

dementia

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5
Q

drug induced tremors could be caused by

A

enhanced physiologicals
parkinsonian treatments
cerebellar treatments
withdrawal from certain substances

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6
Q

induced Tremors by enhanced physiologicals

A

sympathomimetics - bronchdilators, thecphylline, psuedoephedrine
antidepressants
amiodorone
sodium valproate

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7
Q

induced Tremors by Parkinsonian drugs

A

neuroleptics, metoclopramide, prochloperozine, antidepressants, calcium antagonists, sodiun valproate

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8
Q

induced Tremors by cerebellar drugs

A 
Lithium 
phenytoin 
chemotherapy-5FU 
chronic alcoholism 
amiodorone
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9
Q

induced Tremors by withdrawal

A

benzodiazepines
SSRI-paroxefine
alcohol
opiates

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10
Q

serotonin syndrome

A

caused by SSRIs, TCAs, MAOIs through 5HT overstimulation
occurs within 24 hrs
symptoms: autonomic, mental, neurlogical, myoclonus, diarrhea, nausea, shivering
Dilated pupils, myoclonus, hyperreflexia
increased WCC and increased CK
Serious complications: DIC, leukopenia, thrombocytopenia, seizures, multi organ failure, rhabdomyolysis,
Tx by discontinuing or with Benzos, cyproheptodine, chlorpromazine
Recover 70% within 24 hours
23 deaths reported up to 1999

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11
Q

Neuroleptic malignant syndrome

A

caused by neuroleptics, metolopramide, amoxopine (TCA), sudden dopaminergic drug withdrawal through D2 receptor blockade.
symptoms onset within 7 days (longer with depot drugs)
autonomic, mental, neurological, dysphagia, hypersalivation, incontinence, Temp over 38C, akinesia, extrapyramidal rigidity
increased WCC and larger increase in CK
Severe - most cases require intensive care
DIC, acute renal failure, rhabdomyolysis, myoardial infarction, sepsis, cerebellar neuronal degeneration
Tx by discontinue use, dopamine agonists, amantadine, carbidopa-levodopa, dantrolene
recovery in 2-14 days
10-20% of cases

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12
Q

Mechanism of serotonin overstimulation: drugs metabolized to serotonin or promoting serotonin release

A 
Lithium 
MAOIs 
tryptophan 
trazodone
tetrabenazine
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13
Q

mechanism of serotonin overstimulation: inhibition of serotonin reuptake

A

SSRIs, TCAs, trazodone, tramadol, st johns wort, enlafazine

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14
Q

mechanism of serotonin overstimulation: inhibition of serotonin metabolism

A

MAOIs( phenelzine, isocarboxid, selegiline)

st john’s wart

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15
Q

Mechansim of serotonin overstimulation: postsynaptic receptor stimulation

A

buspirone
triptans
lithium
carbamazepine

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16
Q

TCA

A

tricyclic antidepressants

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17
Q

Theoretical ways anesthesia may effect AD pathogenesis

A

Anesthesia causes Abeta oligomerization, Tau phosphorylation, hypothermia (leads to Tau phosphorylation which leads to NFT)
both abeta oligomerization and NFT lead to decrease of synaptic plasticity and ends in Neurodegeneration and cognitive impairment

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18
Q

Prescription abuse

A

non medical use, misuse and abuse of prescription drugs are defined as use of prescription medication without medial supervision for intentional purpose of getting high.
33% of surveyed adolescents were developing symptoms of dependency

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19
Q

Rx drugs commonly abused

A

opiates (morphine, codeine, oxycodone/oxycontin, hydrocodone/vicodin and demerol)
depressants - diazepam/valium, alprazolam/xanax
stimulants - methylphenidate/ritalin, dextroamphetamine/dexedrine
anabolic steroids

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20
Q

Highest rate of abuse

A

Pharmaceutical opioids, cocaine, morphine and derivatives

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21
Q

Age group that sees most Rx opioid overdose deaths

A

45-54 yo

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22
Q

treat mild pain with

A

acetaminophen
ASA
NSAIDs/COX1B

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23
Q

treat moderate pain with

A

codeine/ acet
oxycodone/acet
Tramadol

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24
Q

treat severe pain with

A 
fentanyl 
hydromorphone
methadone
morphine 
oxycodone
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25
Q

General side effects of opioids

A 
nausea
constipation 
somnolence
dry mouth 
pruritus 
hypotension
urinary retention 
respiratory depression
26
Q

Neurotoxic side effects of opioids

A 
myoclonus 
hyperalgesia 
allodynia 
delirium 
hallucinations 
cognitive impairment
27
Q

Opioid induced myoclonus

A

all muscle groups
often best observed when patient sleeping
incidence of opioid related myoclonus varies from 2.7 to 87%
most recognized with metabolites of morphine (particulary M3G), however also seen with opioids with no active metabolites (methadone, fentanyl)

28
Q

opioid neurotoxicity

A

myoclonus-uncontrollable twitching and jerking of muscles or muscle groups, usually occurs in the extremities
hyperalgesia increased sensitivity to noxious stimuli or even light touch
delirium with hallucinations
grand mal seizures-late

29
Q

Neurotoxicity/ Delirium

A

Myoclonus
delirium/agitation
hyperalgesia
hallucinations
intractable nausea
occurs in pts taking opioids in high doses/prolonged periods/who develop renal impairment
pts occasionally present with sudden exacerbation of cancer pain.

30
Q

Opioidd induced hyperalgesia: symptoms

A

pain persists of increasees with increased opioidd dose
pain increases with constant opioid dose
pain worse on opioid treatment than before treatment with opioids
duration of analgesia decreases with duration of therapy
pain becomes increasingly diffuse and less well defined in character with increased dose or duration of treatment

31
Q

Pharmo properties attributable to M3G (+H3G)

A 
central agitation 
hallucinations
myoclonus 
convulsions
coma 
hyperalgesia
32
Q

Pharmo properties attributable to M6G (+H6G)

A 
sedation 
nausea
respiratory depression 
coma 
analgesic effect
33
Q

Factors that increase accumulation of morphine/HDM metabolites

A

Renal failure - urinary obstruction, meds, NSAIDs, ACE, cancers, MM, lymphoma
dehydration
rapid and substantial increases in opioid doses
long term use

34
Q

Hydromorphone

A

5x as potent as morphine - start low with dosing
little difference between hydromorphone and other opioids in terms of efficacy or adverse effects
H3G is metabolite of hydromorphone - dep on renal excretion, no analgesic action, can lead to neurotoxic effects

35
Q

Meperidine

A

short duration of action
associated with delirium in elderly patinets
normeperidine accumulation can lead to neurotoxicity
(grand mal)
being removed from many hospital formularies
Restricted use; post operative shivering/prevention of rigors, short term IM/IV analgesia, avoid use in elderly

36
Q

Spectrum of opioid-induced neurotoxicity

A

opioid tolerance, mild myoclonus, severe myoclonus, seizures, death
opioids increased leads to delirium and hyperalgesia to agitation and mis-interperted pain

37
Q

communication between nerve system and immune system

A

Hard wired synapses - NT and neuropeptides and innervation of lymph nodes
Cytokine-hypothalamic-pituitary-adrenal axis - neuroimmunoendocrine
toll like receptor expression in neurons and endocrine cells of the HPA axis

38
Q

Opiate induced hyperalgesia

A

opioids stimulate mu receptors, Gs coupled opioid receptor, M3 glucuronide

39
Q

Cytokine HPA axis

A

stressors induce pituitary to release ACTH, sympathetic stimulation and prolactin and GH
cytokines are released (IL-1)
Hypothalamus releases CRH, increase in IL-1R, get ACTH and b-endorphin
ACTH leads to Glucocorticoid and enkephalins and catecholamines release which all act to induce release IL-1

40
Q

Glia sustaining pain

A

Distress signals from neurons leads to glutamate, ATP, NO, sub P, fractalkine, potassium ion release that influence microglia which release glutamate, ATP, NO, sub P and BDNF which act on pre and post synaptic neurons and also astrocyte
Inflammatory cytokines act pre and post synaptically

41
Q

opioid use/ drug seeking behaviors

A

psychological or physical dependence
inadequate pain treatment (pseudoaddiction) - tolerance, opioid hyperalgesia, progression of underlying disease process
use of opioids to relieve a comorbid condition - depression, anxiety
search for sympathy, preoccupation with being unwell (professional patient)
addiction

42
Q

Opioid tox -tx steps

A
  1. recognize syndrome
  2. discontinue the offending opioid - Naloxone does not reverse neuroexcitatory effects and may in fact exacerbate them
  3. hydrate to help clear opioid and metabolites
  4. consider benzos to decrease neuromuscular irritability
  5. explore options to address the suffering
43
Q

how to treat opioid neurotoxicity

A

stop opioid or reduce dose if pain allows

start new opioid - Phenanthrene opioids and nonphenanthrene opioids

44
Q

Treat jerking with

A

benzos like clonazepam and lorazepam

45
Q

phenanthrene opioids

A 
codeine
hydrocodone
hydromorphone
morphine 
oxycodone
oxymorphone
46
Q

nonphenanthrene opioids

A

piperidine derviatives - fentanyl, meperidine, sufentanil
buprenorphine
methadone
tramadol

47
Q

discontinue offending opioids

A

simply decreasing the dose only postpones the need to switch opioids
adding a benzos without addressing the opioid ignores potential reversibility
stepwise converison (days) in mild neurotoxicity
abrupt discontinuation if life threatening neurotoxicity (seizures imminent)

48
Q

Hydrate to help clear opioid and metabolites

A

morphine and hydromorphone metabolites are renally excreted
oral,SQ, or IV depends on the severity and venous access
ex of aggressive hydration: NS 500 ml bolus followed by 250 ml/hr plus furosemide 40 mg IV q6H

49
Q

Benzos decrease neuromuscular irritability

A

clonazepam - long acting po
lorazepam - intermediate duration of action p.o, SL, IV, IM -for seizures
midazolam - short acting SQ, IV, SL, IM - generally not used
be cautious with additive respiratory depressant effects if also giving opioids by bolus

50
Q

options to address the suffering

A

switching opioids
steps to decrease opioid requirements adjuvants (gabapentin, corticosteroid, ketamine, bisphosphonates)
Procedural intervention - epidural, spinal, intrathecal catheters
radiation/chemotherapy
orthopedic intervention
seating, positioning

51
Q

challenges in managing pain/distress in setting of neurotoxicity

A

quite possible that a substantial proportion of current offending opioid dose is being targeted at treating opioid induced hyperalgesia or restlessness
-the opioid has been increased to treat its own side effects
tolerance to offending opioid, not “crossed over” to alternatives (incomplete cross-tolerance)
impossible to calculate dose equivalences of alternative opioids conversion charts dangerous to use

52
Q

Treatment of neurotoxicity

A

Hydrate, rotate opioid, treat symptoms/agitation, rule out other causes of delirium, reassess

53
Q

Microtubule inhibitors

A 
vincristine
vinblastine
vinorelbine 
paclitaxel 
docetaxel
54
Q

Vincristine

A

side fx - neurtox, constipation
interactions - phenytoin, phenobarb, carbamazepine, azole antifungal
monitor CBC, hepatic function, peripheral neuropathy

55
Q

Vinblastine

A

side fx - myelosuppression, neurotoxicity

monitor - CBC, hepatic function

56
Q

Vinorelbine

A

side fx - granulocytopenia

monitor - CBC, hepatic function

57
Q

Paclitaxel

A

side fx - neutropenia, neurotoxicity, alopecia, N and V
interactions - repaglinide, gemfibrozil, rifampin (CYP2C8)
monitor - CBC, hepatic function, peripheral neuropathy

58
Q

Docetaxel

A

side fx - neutropenia, neurotoxicity, fluid retention, alopecia, N,V,D
interactions - ketoconazole, ritonavir (CYP3A4)
monitor - CBC, hepatic function, peripheral neuropathy

59
Q

Mitosis is blocked by

A

Vinca alkaloids

paclitaxel

60
Q

Chemotherapy induced peripheral neuropathy - CIPN

A

Duloxetine is the only intervetion with efficacy for the treatment of CIPN demonstrated from a randomized, double blind, placebo controlled trial

BCN EXAM 5 (2 decks)

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