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Pharmacy CPS Flashcards > NEUROLOGY 2: PAIN, HEADACHE & MIGRAINES. DRUG WITHDRAWAL, CANNABIS > Flashcards

NEUROLOGY 2: PAIN, HEADACHE & MIGRAINES. DRUG WITHDRAWAL, CANNABIS Flashcards

1
Q

describe difference between difference types of headache
- tension type headache ( TTH)
cluster headache
migrane

A

see pic

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2
Q

headache that is associated with GI symptoms ( nausea) and/or light sensivitiy

A

migrane

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3
Q

headache that last 4-74 hours

A

migrane

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4
Q

headache that is not worsen by activity

A

TTH

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5
Q

when to refer patient with headache

A 
thunderclap onset 
progressive severity or increased frequency 
systemic illness/ fever
acute glaucoma 
stiff neck. focal signs, reduced LOC 
child or elderly 
temporal arteritis
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6
Q

what is medication over use headache

A

headache with use of simple analgesics >15 days/ month

or opioids, triptans, analgeic-opioid combo >10 days/ month

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7
Q

drugs associated with intracranial HTN leading to HA

A

tamoxifen
tetracycline
isotretinoin

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8
Q

first line for TTH

A

NSAID

( celecoxib - COX2 selective, high risk CV, less GI risk

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9
Q

prophylaxis in TTH

A

1st: amitriptyline, nortriptyline ( 10-100mg/day)
2nd: mirtazapine ( 30 mg/day)
venlafaxine (150mg /day)

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10
Q

cautions for triptans

A

caution when used with serotonergic drugs ( due to increased serotonin syndromes)

  • drugs inducing or inhibiting enzymes
  • do not use in patient with cardiac like symptoms
  • do not use triptan within 24 hrs of another triptan
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11
Q

how often can we use triptan

A

<10 days/ month to avoid medication over use headaches
do not use a triptan within 24 hrs of another triptan

**second dose of triptan unlikely to be effective if 1std dose provided no relief within 2 hrs

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12
Q

CI for triptan

A

heart disease, uncontrolled HTN, pregnancy, bisilar or hemiplegic migraine

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13
Q

AE of triptans

A

chest discomfort, fatigue, dizziness, paresthesias, drowsiness, nausea, throat symptoms.

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14
Q

MOA of triptans

A

All act on serotonin (5-HT) receptors found on blood vessels and neurons to inhibit the release of vasoactive neuropeptides and cause vasoconstriction of the pain-sensitive blood vessels

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15
Q

ERGOT derivatives contraindication

A

CVD, PVD, sepsis, liver/kidney disease, pregnancy, and patient taking potent inhibitors of CYP3A4

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16
Q

prophylaxis for migraine

A

beta blocker ( 1st line) propranolol ( best studies), metropolol, nadolol and atenolol ( fewer CNS SE)
TCA: amitriptyline, nortriptyline ( consider if depression, insomnia or TTH)
venlafaxine
candesartan
valproic/ divalproex, topiramate ( if overweight)
lithium
fovastriptan ( menstrually associate migraine)

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17
Q

migriane and pregnancy

A

non pharm 1st choice
acetaminophen NSAID ( avoid if possible, especially in 3rd trimester)
prophylaxis: propanolol
**no triptan and especially ergot, and topiramate

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18
Q

migraine and breastfeeding

A

acetaminophen
ibuprofen if NSAID preferred
sumatriptan
prophylaxis: propanolol, magnesium citrate

**avoid ergot, barbiturates and opioids

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19
Q

which triptan is useful for preventing menstrual migraine

A

Frovatriptan, naratriptan and zolmitriptan

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20
Q

cox 1 and cox 2 inhibition

A

Cox 1: anti platelets effects
Cox 2: analgesic, anti-inflammatory and antipyretic effects

COX 2: celecoxib, diclofenac *( increased affinity for COX 2 but retain cox-1 acitivity)

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21
Q

which NSAID has highest CV risk among the semi/non-selective agents

A

diclofenac PO

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22
Q

CI of NSAID

A

< 18 Y/O with chicken pox, influenza, or flu like symptoms ( risk of reye syndrome)

  • hypersensitivity
  • 3rd trimester of pregnancy
  • active peptic/ulcer, IBD
  • severe renal impairment
  • severe uncontrolled heart failure

BARS: bleeding, asthma, renal , stomach
- known hyperkalemia
-

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23
Q

which NSAID cannot be used in breast feeding

A

-celecoxib, diclo, indomethacin,

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24
Q

AE of opioids

A
  • sedation, N/V, constipation
  • respiratory and CNS depression
  • pruitis if natural opioids ( morphine)
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25
Q

AE of gabapentin, pregabalin

A

sedation, weight gain, dizziness, peripheral edema

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26
Q

what is bell palsy

A

unilateral weakness of facial paralysis usually linked to a viral infection

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27
Q

risk factors of bell palsy

A

diabetes, hypertension, URTI, obesity, pregnant women ( 3rd trimester), pre-eclampsia

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28
Q

treatment for bell palsy

A

corticosteroid ( pred 60mg x 5 days, then taper over another 5 days for a total of at least 450 mg)

ARV+ corticosteroid in patient with severe paralysis or immunocompromised
ARV alone is not recommend

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29
Q

AE corticosteroids

A

hyperglycaemia, GI upset, mood swings, hypocalcemia, hypokalemia, sodium and fluid retention

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30
Q

what is guillain barre syndrome ( GBS)

A

autoimmune
body’s immune system attacks the nervous system often preceded by an infection causing weakness and paralysis of the limbs

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31
Q

bells palsy in children

A

steroid is not recommend there is no demonstrated benefit from corticosteroid

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32
Q

treatment for GBS

A

plasma exchange and immunoglobulin

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33
Q

when should we administer immunization after GBS

A

withheld for one year

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34
Q

difference between CB1 and CB2

A

CB1 :
abundant in CNS, involved in hemostasis, motor control, cognition, emotional responses, motivation

CB2: immune systems and blood cells, involved in an immune and inflammation response

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35
Q

difference b/w THC and CBD

A

`THC: psychoactive effects, partial agonist at CB1 and CB2 receptors, releases dopamine in the brain

CBD: no binding to CB1 or CB2
produces physical effects
anti-inflammatory, analgesic, anti-emetic, anti- epileptic properties

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36
Q

evidence on cannabis are on the following medical conditions

A

pain: refractory neuropathic pain or refractory palliative cancer pain
N/V: refractory CINV

SPASTICITY: refractory spasticity in MS and SCI

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37
Q

what are the cannabis act

A

possess up to 30g of legal cannabis ( DRIED or equivalent in non-dried form)
share up to 30G with other adults
4 cannabis plant per residence for personal use

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38
Q

cannabis dosing

A

0.5-1g/ day starting and average dose of 1-3 g/ day

no evidence based dosing recommendations at this tie

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39
Q

2 cannabis product are available in canada

A

nabilone and tetranabinex/nabidiolex

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40
Q

what is the indication for nabilone

A

severe N/V from cancer chemotherapy

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41
Q

indication for sativex

A

adjunctive relief of advanced cancer pain and MS pain

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42
Q

does nabilone contain CBD

A

yes 1mg= 10 mg THC

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43
Q

cannabis AE

A

CNS: psychosis, hallucinations
CV: tachycardia, arrhthymias
GI: decreased gastric motility
reproduction: anti-androgenic effects, decreased sperm count and motility

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44
Q

cannabis drug interactions

A

significant with CNS depressants
metabolized b CYP3A4 and CYP2C9
induces CYP1A2

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45
Q

are stimulants recommend for chronic fatigue syndrome?

A

no

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46
Q

when should muscle spasticity be treated

A

should not always be treated as it can worse a patient gait and movement. treat only when it causes pain and interferes with the daily function

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47
Q

treatment for generalized spasticity

A

baclofen ( first line)
tizanidine ( second line in combo with baclofen)

Gabapentin ( not canada approve indication) but useful if there is neuropathic pain

BZD: helpful for treating nighttime spasms

Cannabinoids: beneficial add on- improves neuropathic pain, sleep disturbance and spasticity

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48
Q

treatment for focal spasticity

A 
phenol injections ( repeated q6months) 
onabotulinumtoxin A ( botox) - q 3months
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49
Q

clinical presentation of moderate-severe drug withdrawal syndromes

A

seizures, hallucinations, delirium tremens ( DT)- mortality 5%

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50
Q

supportive care for AWS

A

IV fluids
replenish electrolytes
nutritional supplementation

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51
Q

why is thiamine and glucose given in AWS supportive care

A

prevents wernicke’s encephalopathy

52
Q

first line pharmacotherapy for AWS

A

BZD- preventing seizures, hallucinations, agitation, tremors, autonomic hyperactivity

**dosing via CIWA-AR score

53
Q

when is intermediate acting and long acting BZD appropriate?

A

intermediate: Lorazepam, oxazepam
more suitable for elderly and liver dysfunction

Long acting BZD: less risk of rebound effects or withdrawal seizure, useful in high risk patient with prolong symptoms
chlordiazepoxide, diazepam

54
Q

score for alcohol withdrawal and opiate withdrawal

A

CIWA-AR ( alcohol)

COWS ( clinical opiate withdrawal scale)

55
Q

how long after opiate cessation will you start to feel symptoms of withdrawal

A 
short acting ( heroine)- 8-24 hours of last dose 
long acting opioids ( methadone) 12-48 hours after last dose
56
Q

first line therapy for opiate withdrawal

A

Buprenorphine/naloxone ( Suboxone)- for detoxication and maintenance

safer than methadone ( lower risk of respiratory depression) but can precipitate opioid withdrawal symptoms

57
Q

2nd line for OW

A

methadone- long acting 24-36 hrs

58
Q

agent used to decreased sympathetic activity of withdrawal

A

clonidine ( blunts autonomic withdrawal symptoms ( sweating, abdominal craps, chills, anxiety, insomnia and tremor)

59
Q

AE of clonidine

A

sedation, dry mouth, orthostatic hypotension**

60
Q

how long after BZD cessation will you start to feel symptoms of withdrawal

A

short acting: after 12-24 hrs of last dose

long acting: 5 days ( peak 1-9 days of the last dose

61
Q

score to assess withdrawal severity for BZD

A

CIWA-BENZO

62
Q

therapeutic approach in BZD withdrawal

A

titrate to effect with long acting BZD, then taper over a few months

63
Q

therapeutic approach to stimulant withdrawal

A

no approved medication

? potential methylphenidate may be used as maintenance therapy

64
Q

what is MS and explain the pathophysiology

A

chronic neurologic disease in which the body’s immune system damages its own nerve cells (myelin destruction) and connections b/w the brain and spinal cord

65
Q

clinical presentation of MS

A

numbness, weakness, fatigue, cognitive difficulties, ataxia, optic neuritis, bowel/bladder abnormalities and neuropathic pain.

66
Q

which environmental factor are associated with increased risk of MS

A

deficiency of Vitamin d ( especially in pregnancy or in neonates)

67
Q

initial presentation of MS

A

80% of patient present with clinically isolated syndrome

ypically presents as unilateral optic neuritis, partial myelopathy or focal syndromes

68
Q

list 4 subtypes of MS

A 
clinically isolated syndrome ( CIS) 
relapsing- remitting MS ( RRMS) 
secondary progressive MS (SPMS) 
primary progressive MS ( PPMS) 
Progressive relapsing (PRMS)
69
Q

what is PPMS (primary progressive MS), how it is different from secondary progressive MS

A

primary: 10-15% onset, neurologic disability that steadily worsens from disease onset , no distinct period of remission or relapse

SPMS- progressive that follows after RRMS
symptoms slowly worsen with viable remission and relapses

70
Q

is there a cure for MS, what is the role of DMT ( disease- modifying therapies)

A

no

reduce relapse rate in RRMS ( relapsing- remitting)

no role/ no impact on PPMS or SPMS unless patient have a progressive disease with frequent relapses

71
Q

first line DMTs for MS

A

interferon beta: standard first line, reduces relapses rate and # of size of MRI detectable lesions , reduce conversion

glatiramer actate: reduces relapse rates ( does NOT prevent disease progression) and reduces MRI detectable lesion

Dimethyl fumurate: activates nuclear factor like 2 pathway, reduces the # and rate of relapses

teriflunomide: reduces B and T cells; reduces relapses rate and disease progression teratogenenity

71
Q

2nd line DMT for MS

A

High efficacy therapy: more efficacious than first line but increase toxicity: “early intensive therapy “

ocrelizumab: approved for PPMS and arms

alemtuzumab life-threatening and fatal cases of autoimmune hepatitis, hemophagocytic lymphohistiocytosis and cardiovascular reaction
cladribine- higher grade lymphopenia, which is linked to herpes zoster infection.

fingolimod - skin cancer, variella zoster infection, macular weeks

Siponimod: active SPMS only

natalizumab- case of PML

72
Q

which drug can be used to reduce length and severity of acute relapses in MS

A

high dose methylprednisolone 1G IV daily for 3-5 days (short term) followed by oral prednisone for a few days

** this regimen does not have an effect on the disease course**

73
Q

what is the time to effect for interferon beta?

A

3 months

74
Q

drug use increases what in the brain

A

dopamine- responsible for feelings of pleasure or euphoric effects
- reinforces our behaviour to report pleasurable activities

75
Q

list drugs that are consider stimulants

A

cocaine, amphetamine, methamphetamine, methylphenidate, nicotine, caffeine

76
Q

1st and 2nd line treatment of OUD?

A

1: suboxone
2: methadone

77
Q

normal dose of suboxone

A

2-24 mg/ day once daily or alternate day dosing

78
Q

AE of suboxone

A

headache, decreased libido, constipation, sweating

79
Q

what is the role of naloxone in combo with buprenorphine?

A

to deter crushing and injecting subxone

80
Q

what is sublocade and when can it be administered?

A

sublocade is buprenorphine extended release SC injection ( once-monthly)
patient must be stabilized on subocone for at least 7 days and must be between 8-24 mg
** starting dose is 300mg monthly x 2 months then MD 100mg x monthly

81
Q

when is buprenorphine subdermal implant indicated?

A

delivers buprenorphine continuously for 6 months

indicated for patient clinically stabilized on 8mg or less of trans mucosal buprenorphine per day
And stabilized on SL for 3 months prior to starting

82
Q

MOA of suboxone and methadone

A

buprenorphine: partial mu opioid agonist and weak kappa antagonist, naloxone is opioid antagonist
methadone: full opioid agonist

83
Q

AE of methadone

A

QT prolongation, sedation, sexual dysfunction, constipation

84
Q

advantages and disadvantages of suboxone and methadone

A

suboxone: less risk of overdose ( ceiling effect), shorter time to achieve therapeutic dose, fewer drug interactions

Dis: suboptimal for individuals with high opioid tolerant

methadone: better treatment retention, no max dose ( high opioid tolerance patient), easier to initiate treatment

Dis: many drug interactions, higher risk of QT prolongation, higher risk of overdose

85
Q

how handle missed methadone dose:
missed 1-2 days, 3 days, 4 or more

**how to deal with emesis

A

1-2: give as usual
3 days, need to be assessed by MD, do not provide dose until seen by MD
4 or more: major loss of tolerance, see MD and may restart on low initial doses

emesis: not replace unless observed by pharmacy staff
<15 mins: replaced
>15 mins: not replaced

86
Q

what is used for opioid overdose

A

naloxone ( duh!)

87
Q

when can u repeat naloxone dose?

A

3 mins if first dose does not work

88
Q

OUD in pregnancy and breastfeeding, what can be used?

A

preg: ??methadone ( risk/benefit must be evaluated), buprenorphine ( safe)
beastfeeding: methadones and buprenorphine safe

89
Q

does naloxone reverse overdose cause by BZD, stimulants and alcohol?

A

NO, opioids only

90
Q

1st line treatment for alcohol use disorder?

A

acamprosate: glutamate antagonist- indicated in patient with hepatic insufficiency, cannot used in severe renal impairment, reduce dose between 30-50 ml/min
naltrexone: opioid antagonist - decreased euphoria and cravings related to drinking alcohol. cautions in patient with hepatic dysfunction

91
Q

when can you start acamprosate and naltrexone

A

acamprostate: >/ 4 days of alcohol abstinence
naltrexone: opioid free for >/ 7 days prior to initiation

92
Q

2nd line for AUD?

A

disulfiram: causes a disulfiram reaction within 12-24 hours of drinking - aversive therapy

topiramate, gabapentin

93
Q

which MS drug cannot be used in pregnancy

A

teriflunomide

94
Q

which MS drug have interaction with warfarin

A

Teriflunomide ( decreases INR)

95
Q

which MS medication can cause blue-green discolouration of the urine

A

mitoxantrone

96
Q

important counselling points for dimethyl fumarate

A

avoid live vaccines such as measles, mumps and varicella

97
Q

what is consider chronic pain

A

pain lasting >3-6 months

98
Q

nociceptive pain is separated into what

A

somatic pain ( skin, bone, joint, muscle or connective tissue), visceral pain ( in the internal organs)

99
Q

place in therapy for duloxetine in pain

A

1st line peripheral diabetic neuropathy and fibromyalgia

100
Q

place in therapy for opioids

A

3rd line for severe nociceptive pain or Neuropathatic ( adjunctive)

101
Q

if GI risk is the primary concern, use what NSAID

if CV risk is the primary concern?

A

GI risk: celecoxib+ PPI

CV risk: naproxen +PPI

102
Q

which opioid is effective for neuropathic pain

A

tramadol

103
Q

what is the opioid dose for breakthrough pain

A

about 10% of total daly dose and order q1h prn

104
Q

opioid drug interactions

A

Serotonin drugs, respiratory depressant ( BZD, alcohol) CNS depressant

105
Q

know morphine equivalence conversion

A

see pic

106
Q

what is the difference between adaptive vs maladaptive pain?

A

nociceptive and inflammatory pain is adaptive. Maladaptive becomes disengaged from noxious stimuli or healing and is chronic. EX: IBS, fibromyalgia

107
Q

what is an adequate trial of gabapentin

A

2 months

108
Q

which TCA have the most potent anticholinergic effectst

A

amitriptyline, desipramine has the least

109
Q

which opioids should be avoided in chronic kidney disease

A

morphine, codeine and meperidine

HM, fentanyl, methadone and buprenorphine can be used

110
Q

max dose of MEQ daily

A

90 mg

111
Q

which opioids reduce seizure threshold

A

tramadol

112
Q

methadone should not be titrated more than?

A

5-7 dyas

113
Q

which agent have a canada approved indication for chronic migraine?

A

Botulinum toxic

114
Q

what is the official indication for propranolol in migraine

A

episodic migraine prophylaxis

114
Q

what is the official indication for propranolol in migraine

A

episodic migraine prophylaxis

115
Q

is codeine recommended for patient <12 years old?

A

NO

116
Q

clinical pearls for tramadol

A

1) related to morphine and codeine
2) has less abuse potential than opioids
3) 2 postulated MOA
Tramadol’s metabolism is variable and unpredictable.
Toxic effects include seizures and serotonin syndrome.

117
Q

what is the recommended dose of naloxone iV

A

0.4 to 2 mg IV every 2-3 mins.

118
Q

what opioid has significant life threatening interaction with MAOI

A

meperidine

119
Q

what is the dose recommendation for morphine in a child?

A

0.01 to 0.05mg/kg/hour

120
Q

how often can topical diclofenac be applied

A

QID for effectiveness

121
Q

what is the approach with chronic non cancer pain with active substance use disorder?

A

Opiates is not recommend. sing acetaminophen and an NSAID is a start, however this patient needs to be reassessed since it may not be enough for pai

122
Q

what is the recommended tapering regimen for opioids

A

the rate of taper can vary from 10% of the total daily dose every day, to 10% of the total daily dose every 1-2 weeks. Slower tapers are recommended for patients who are anxious about tapering, may be psychologically dependent on opioids, have co-morbid cardio-respiratory conditions, or express a preference for a slow taper. Once one-third of the original dose is reached, slow the taper to one-half or less of the previous rate

123
Q

if one opioids such as morphine did not relieve back, would switching to another opioid such as HM help?

A

there is no evidence for switching to opioid will relieve pain

124
Q

why is naloxone not given orally for overdose?

A

Although absorbed readily from the GI tract, naloxone is almost completely metabolized by the liver before reaching the systemic circulation and thus must be administered parenterally.

125
Q

Which MS drug with highest PML

A

Natalizumab

Pharmacy CPS Flashcards (27 decks)

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