Week 7: ADHD, Neuro Pain Flashcards
Mechanisms of Pain
Nociceptive
a, stimulation
*bradykinnins, K+, prostalglandins, histamine, leukotreines, seretonin, substance P, etc.
b.transmission
*a delta fibers: sharp localized pain-myelinated
*C fibers-unmyelinated -dull ache
Perception
Modulation
*endogenous opiate system (enkephlins, dynorphins, beta endorphines) and mu, delta, and k receptors
*NMDA receptors decrease effects of opioids
*seretonin, NE, GABA, neurotensin
CDC guideline for prescribing opioids for chronic pain
- recommend non pharm and non opioid treatments prior to opioids ; if opioids used, combine with non-opioids as appropriate
treatment goals should be established before initiating therapy. continue opioid only if improvement function/pain more than risks to patient
providers should weigh the potential risks versus benefits and discuss them w. patients when initiating opioids. pts should aldo be monitored periodically during treatment
neuropathic pain .
Pain caused by a lesion or disease of the somatosensory nervous system.
neuropathic pain is a clniical description (NOT) a diagnosis
characteristics of nervous system damage
increased nerve cell firing
AND/OR
decreased inhibition of neuronal activity in central structures uaually due to deafferentation
AND/OR
intact circuitry at the central level but a gain in response (sensitization) such that normal sensory input is amplified and sustained
Presentation / assessment of neuro. pain
spontaneous transmission
*continous (burning,throbbing,aching,shooting)
*intermittent (episodic, paroxysmal). shooting,stabbing,orelectric shock-like
hyperalgesia
increased pain from a stimulus that normally provokes pain
allodynia
*pain de to a stimulus that does not normally provoke pain
neuropathic pain general treatment principles
trt directed at reducing/stabilizing nervous system activity
drugs effective in 1 or more neuropathis syndromes are reasonable choices for neuropathies
onset of action: may be days to weeks
*dont expect this to act like an prn med for headache”
NEUROPATHIC PAIN TREATMENT
Tricyclic AD(TCA’s)
examples:
advantages:
disadvantages
dosing
examples: secondary (nortriptyline, desipramine)
tertiary (amitrityline, imipramine (crosses BBB)
advantages:
*most data
once daily dosing
concaminnant insomnia, depression’
disadvantages
delayed onset
anti-ach, cardiotoxicity
dosing
25 mg hs, max 150mg/day
trial: at least 6-8 weeks, 2 weeks @ max dose
NEUROPATHIC PAIN TREATMENT
SNRI
examples:
advantages:
disadvantages
dosing
examples:duloxetine, venlafaxine, DRIZALMA (only fda approved duloxetine DR capsule to be opened and sprinkled)
advantages:duloxetine fda approved in PDN, fibromyalgia
concamminant depression
side effect profile
disadvantages
risk of seretonin syndrome +/- interacting meds
duloxetine CI in hepatic impairment. severe end stage renal diseaSE (<30mL/min)
dosing:
D-30 mg 1x day, max 60 mg 2xday
v- 37.5 1-2xday, max 225 mg/day
NEUROPATHIC PAIN TREATMENT
SNRI
Milnacipran (Savella)
indication: fda approved fibromyalgia in 2009
37% pf subjects report ~50% decreased in pain
MOA: SNRI-3:1 NE:5HT
nmda receptor binding
lacks histaminic and muscarinic activity
pro:well tolerated, can improve fatigue
cons: bid
HTN
dosing: start 12.4 faily, titrate over 1 week to 50 mg bid
max 100mg bid
NEUROPATHIC PAIN TREATMENT
alpha 2 delta ligands
aka gabapentinoids
modulates hyperexcited nuerons by
…
*binds to presynaptic neurons at the a2 delta subunit of voltage gated calcium channels
drug binding reduces calcium influx into presynaptic terminals
decreased calcium influx reduces excessive release of excitatory neurotransmitters (eg. glutamate, substance P, noradrenaline
NEUROPATHIC PAIN TREATMENT
Gabapentin
examples:
advantages:
disadvantages
dosing
examples:
advantages:
low incidence of DI’s and ADRs
FDA approved for post herpatic neuropathy
disadvantages
mild cns depression,
significant toxicity
renal dosing
*Crcl: >60 mL/min: no dose adj. needed
Crcl: 30-59 total dose range 400-1400 mg/day PO in evenly divided doses
*CRcl>15-29 mL/min: total dose range 200-700 mg/day PO given in one daily dose
*Cecl=15 mL/min: total dose range 100-300 mg/day PO given in one daily dose at 100, 125 , 150, 200, or 300 mg
Crcl <15: reduce daily dose in proportino to crcl (e.g crcl=7.5 mL/min recieve 1/2 dose of pts. w. crcl 15mL/min recieve)
dosing
NEUROPATHIC PAIN TREATMENT
gabapentin products and dosing
gabapentin oral capsule, tablet, and solution
300 mg 3x/day start
lower in renal impairment-100mg 2-3x/dau
max 3600 mg/day
variable onset of action
gabapentin oral tab ER (Gralise 300 mg tab)
once daily eveneing meal
titrate to 1800 mg/day
gabapentin enacarbil oral tab ER (Horizant)
twice daily x3 days, then 2 tabs twice daily.
max 1200 mg/day
NEUROPATHIC PAIN TREATMENT
Pregablin
examples:
advantages:
disadvantages
dosing
examples:
advantages:
low incidence on DIs and ADR
concaminant anxiety
fda indicated in PDN, PHN and fibro.
disadvantages
DEA schedule V-dependency, euphoria
mild CNS depression, significant in toxicity
renal insufficiency
dosing
150 mg/day start: divided doses either 2x or 3x a day
lower in renal impairment
titrate q 3-7 days by 150 mg/day if tolerated.
max 600 mg/day
NEUROPATHIC PAIN TREATMENT
TRamadol
examples:
advantages:
disadvantages
dosing
examples:
advantages:
moderate pain (weak mu agonist),
less resp. depression
abuse potential
secondary moa of inhibiting reuptake of NE ans 5HT
disadvantages
DI: carbamezapine, quinidine, TCA, SSRIs
se: dizziness, GI, constipation, seizure risks
dosing
NEUROPATHIC PAIN TREATMENT
Tapentadol (Nucynta)
examples:
advantages:
disadvantages
dosing
indication: neuropathic pain associated w. peripheral neuropathy
examples:
advantages:
mu agonist
NE reuptakr inhibition
no active metbaolites
disadvantages
DEA schedule II
dosing
50mg, 75mg, 100mg
q4-6 hrs
1st dose load may repeat once 1 hr after dose
NEUROPATHIC PAIN TREATMENT
Capsaicin
examples:
advantages:
disadvantages
dosing
EXAMPLE: cApsaicin
depletes and prevents reaccumulation of substance p in peripheral sensory neurons
fda approved
application issues
longterm use
otc products can advertise use in arthritis pain, btu can be used in other neuralgias too
NEUROPATHIC PAIN TREATMENT
available forms of Quetenza
Capsaicin 8% topical patch (PHN-RX only)
pretreat w. local anesthetic to treatment area plus 1-2 cm of surrounding area
use up to 4 patches per application ; patches should be applied for 60 min and repeated no more frequently then q3 months as needed
medicated 0.025% patch
zostrix neuropathy 0.25% topical cream
capsaicin topical cream (0.025-0.1%)
NEUROPATHIC PAIN TREATMENT
Lidocaine
indication:
onset:
duration:
dosing
indications: PHN, topical anesthesia (skin mucous membranes, stomatitis)
onset: 5-10 min
duration: variable
how supplied
rx(patch 5%, viscous soln 2%)
otc (up to 4%)
NEUROPATHIC PAIN TREATMENT
medical cannabis
studies found a “significant, but clinically small, reduction in mean numerical rating scale pain scores”
Very general Tratment approach to neuropathic pain and considerations
first line drugs
1.SNRI’s
2.TCA’s
3. Gabapentinoids
consideration: can be used for all neuropathic pain conditions
second line drugs
1.tramadol
2.capsaicin 8% patches
3. lidocaine patches
considerations: tramadol indicated for all. capaicin and lidociane indicated for peripheral neuropathic conditions.
lidocaine has high tolerability and safety
third line drugs
1.strong opioids
2.botulinum toxin
Painful Diabetic Neuropathy (PDN)
patho
damage to peripheal nerves causes hyperexcitability and spontaneous impules
abnormal electrical connections
coupling of sympathetic and aferent neurons and abnormal release of substance Pfrom A fibers
persistent nerve stimulation acivates NMDA receptors
Painful Diabetic Neuropathy
tratment
- increase NE and 5HT increase pain supression induced by the descending inhibitory pathways
- TCAs
also monoamine reuptake, nmda blockade and sodium channel interferance. - SNRI
*duloxetine and venlafaxine
4.a2 delta ligands*gabapentin and pregablin
General proposed treatment algorithm for PDN
PDN
1. Depending on CI’s and co morbidities…can use
a. A2 delta agonists (Pregablin or gabapentin)
*usually first line
b.SNRI’s
c.TCA’S
2.if pain is inadequately controlled and depending on contra-indications a.can use combo therapy.
a.optimize dose of monotherapy and provide adequate duration of therapy
b.add agent from class of drug w. distinctly different pharmacology
ex: if started on a2d ligant, add SNRI or TCA
if onSNRI, add a2d ligand
- if pain is still inadequately controlled
*opioid agonist as monotherapy, followed by combo therapy if pai ncontroll is inadequatey
Post herpetic neuralgia (PHN)
ractivation of varicella-zoster virus
(shingles)
distribution along dermatomes
ften causes PHN d/t sensory nerve damage, causing reduced neurite densities
Treatment of PHN
- TCAs teatment of choise
2.antipileptics
*gabapentin
a.Gralise ER tab-titrate t o1800mg once daily
horizant-gabapentin
Enacarbil ER 600 mg tab 2xday-prodrug
*pregabin
*divalproex
3.Tramadol
4.opioids (oxycontin)
5.lidocaine
5. capsaicin
Low Back Pain
5th most common office visit reason
acute vs. chronic+/- neuropathic
patho:
not necessarily neuropathic, but can turn neuropathic.
soft tissue of lower back damage causes a dysfunctional movement pattenr. decreased local motion, atrophic fibrosis, decreased oxygenation of tissue.
increased locomotion causes microtrauma inflammation and increased release of pain neurotransmitters
causes decreased descending pain inhibition and increased perceved pain. (NEUROPATHIC COMPONENTS) causing fear ofmovement, AND A VICIOUS CYCLE
mangement of low back pain
Self care
nonpharm:usually for chronic(>4 weeks) such as exercise therapy, massage, accupuncture, yoga, cbt, progressive relaxation, intensive interdisciplinary rehabilitation
pharm:
1st line: NSAIDS and APAP(possiblly
can also use skeletal muscle relaxants, TCA’S, trmadol(has nociceptive as well as neuropathic pain mangement proprties), opioids
Fibromyalgia
enhances sensitivity to stimuli. heat and cold
pain is described as a constant dul ache in all 4 quadrants of the body
often accompanied w. fatigue and sleep disturbances and other comorbidities(aka fibromyalgia fog)
patho: abnormalities in neuroendocrine system and autonomic system.
possible genetic risk factos (5ht, comt)
ENVIRONMENTAl triggers, physical psychosoical stessors, such as physical injruy, surgery, acute injuries etc.
central sensitization
dx criteria of fibromyalgia
- widespread pain index (WPI)>/= 7 and symptom severity scale SSS score >/= 5 or WPI or 4-6 and SSS>/=9
2.generalized pain defined as pain in at least 4 or 5 regions must be present. jaw, chest, and abdominal pain are not included in geenralized pain definition
- symptoms havebeen generally presen for atleast 3 months
- a dx of fibromyali is valid irrespective of other dx. a dx of fibromyalgia does not include the presence of other clinically importnt illnesses
pharm treatment of fibromyalgia
amitryptiline (at low dose)
duloxetine or milnacipran(can also relieve fibromyalgia fog)
prgablin
cyclobenzaprine
comprehensive algorithm for the pharm management of neuropathic pain
once dx neuropathic pain
FIRST LINE: 4-6 WEEK TRIAL
a.TCA’s
b.SNRI’s
c.gabapentinoids
d.Topicals (Focal NP)
SECOND LINE: 4-6 WEEK TRIAL
a.tramadol
b.combo 1st line therapy
3RD LINE: specialist refferal
a.SSRI’s/ anticonvulsants, NMDA antagonists
b.interventional therpapies
4th LINE: neuromodulation
5th line: low dose opioids
6th line: targeted drug delivery
Risks and prognostic factors of ADHD
gener: Male>female
ethinicity: black non-hispanic> white non-hispanic>hispanic>asian nonhispanic
genetic and physiological
*elevated risk if first degree relative dx
minor physical anomalies(hypertelorism, highly arched palate, low set ears)
motor delays and neurological soft signs
verly low birthweight 2-3x greater risk ADHD
environment:
fetal alcohol syndrome
lead poisoning
menningitis
obstetri adversity
maternal smoking
adverse parent-child relationship
PTSD
Patho of ADHD
- cortical thinning and delay in cortical thickness, causing reduced activity in prefrontal and anterior cingulate cortex.
2.default mode network over-activity..
and others
SS of ADHD
inattention: wandering off tasks, lacking persistence, having difficulty sustaining focus, being disorganized
- hyperactivity: excessive motor activity, fidgeting, tapping, talkativeness, extreme restlenessness
- impulsivity
desire for immediate rewards or inability to delay gratification
social intrusiveness, making important decisions without considerations of long term consequences
differential dx fADHD
learning disability
siuation stressors
oppositional defiant disorders
conduct disorder
tICS
SLEEP DISORDERS
MOOD DISORDERS
CAN present possible problems because these can present as comorbidities as well
ADHD dx
onset of symptoms must b before 12 YEARS OF AGE
significant impairment must be seen in> 2 settings (i.e home, work, school) and symptoms must be documented
evidence that symptoms interfere w. or reduce the quality of social , acedemic, or occupation functioning
symptoms are not due to other psychiatric disorders, are not better explained by another mental disordrm and are not due to substance use/ intoxication
dx of inattention / hyperactivity (impulsivity)
6 or mor of the following symptoms must be present for atleast 6 months that are inconsistent ith developmental level and that negatively impacts dirctly on social and acaemic / occupational activites
for older adolescents and adults (?17 y.o) atleast 5 symptoms
presentation types of ADHD
combing-criteria met for both inattention and hyperactive/ impulsive
predom. inattentive: criteria nly met for inattention
predom. hyperactive/impulsivity-criteria only met for hyperactive impulse
presentation of ADHD in adults
inattention (hyperactive/impulsive symptoms are associated w. higher rates of comorbid bipolar disorder)
cognitive defecits
impatient
greater risk of unemployment, unstable relationships, psychiatric hospitlizations, and incarcerations
presentation of ADHD in school age children (age 6-11)
difficult academically
combined inattentive and hyperactive impulse
comorbid oppositional and defiant disorder, conduct disorder, and aggression
*child at greater risk for delinquency and SU in adolescence.
most dx are made ~age 7
functional consequences of adhd
delays in language, motor, or social develoment
low frustration tolerance; irritability and mood lability
impaired work/ school performnce
sociall rejection in childhood and adolescence
elevated incidence of interpersonal conflicts w. family, peers, spuses
by early childhood: increased risk of suicide attempts
increased prevelance of substance use disorders SUD
Non pharm treatment of adhd based on age gorup
preschool/school age:
parent/family education of adhd
training on behaviormal modification
behavioral classroom management
adolescent: preakup assignments into mageable segments, structure schedule, behavioral peer interventions (bpI)
ADOLESCENT/ ADULT: ADHD SPECIFIC COGNITIE HAVIOR THERAPY
metacognitive therapy
general treatment principle for trt of ADHD
COMBO NON PHARM AND STIMULANTS HAVE greater improvements in academic/ conduct measures tan either intervention alone
General trt algorithm for ADHD
if pt is predom ADHD presenting
ADHD dx confirmed-> DOES PT HAVE ANOTHER PSYCH DX. WHICH IS PREDOMINANT FOR CAUSING DECREASED QOL
A.predom ADHD: STIMULANTS
1.methylphenydate or dexmethylphenidate(preffered in children 2-6 y.o)
2.dextroamphetamines or mixed amphetamines.
*notes: can start w. either or. if failed one, can use other
a. if inadequate response to stimulants OR if active substance abuse since stimulants have potential for abuse
atomoxetine, viloxazine, guanfacine ER, clonidine ER, buproprion
a.if inadequate response again..
*consider combo trt or TCA
General trt algorithm for ADHD
if pt has predom. comorbid presenting symptoms
- Tourettes
a.treatment: dopamine antag. or a2 agonist
b.some response:add sitmulant, atamoxetine, or a2 agonist.
c.inadequate response: alternative dopamine antag. or a2 agonst - bipolar disorder and/or severe aggression
a.treatment: atypical APS, lithium, or anticonvulsant
b.some response: add stimulant
c.inadequate response: alternative or additional mood stabilizer - anxiety or depression
a.treatment: Antidepressant
b.some response: add stimulant
c.inadequate response: alternative antidepressant
pearl for comorbid ADHD and bipolar treatment
ALWAYS MANAGE BIPOLAR DISORDER FIRST
RISK OF INDUCING MANIC OR HYPOANIC EPISODE W. treatment of stimulants or atomoxetine or viloxazine in uncontrolled BPD
Stimulant considerations
1st line therapy
options: mathylphenydate and amphetamines
amphetamines more potent
lack of respons to one class does not mean lack of response to another sue to diff MOAs.
pros of IR release: lower cost, less insomnia, fewer growth related ADR
pros of ER: med adherance
stimulants
moa
GENERAL DOSING
AE:
DDI
moa: block dopamine and NE reuptake
*amphetamines also increase catecholamine release
inhibit Monoamine oxidase
dosing: titrating to max benefit w. minimum side effects
IR formulations:
dose:BID-TID
drug onset 15-30 min
duration 2-6 hrs
pros : lower cost, less insomnia, fewer growth related ADE
long acting / extended release formulations
QDAY
8-12 hr symptom control
pros: med adherance
AE:
psychiatric: psychosis/mania, agression/violent behavior, severe anxiety/anxiety attacks
cardiac: increased HR~5 pbm, increased BP by 2-7 mmhg
20% increased risk for ED visits
Growth: ~1cm/yr decrease over 1-3 yrs, 3kg weight defecit in 1st year (1.2kg in 2nd year)
DDI: additive effects w. other sitmulants
maoi should not be used within 14 days
mph can increase tca conc.
antacids, ppis, and h2ra can increase absoprtion of mph ir formulations and reduce XR formulations
antacids reduce amp excr., ppis inc. rate of absorption of amp
acidic agents like fruit juce dec. absorption of amp
cyp2d6 inhibitors incr amp salt exposure
alcohol can cause stimulant dumping
adverse effect management of stimulants
1.reduced appetite/weightloss
- stomach ache
- insomnia
- headache
- rebound symptoms
6.inrritiability / jitteriness
1.reduced appetite/weightloss: high calorie meals when stimulant effect is low (breakfast/bedtime) cyproheptadine @bedtime
- stomach ache: take on full stomach, lower dose
- insomnia: give dose earliler in the day, lower last dose of day/ give earlier, add sedating meds @hs (guafenicine, clonidine, melatonin, or cyproheptadine
- headache; divide dose, give w. food, or gve an analgesic
- rebound symptoms: long acting stimulant, atomoxetine, antidepressent
6.inrritiability / jitteriness: assess for comorbid condition, reduce dose, consider mood stanilizer or atypical APS
uncommon stimulant side efects and what to do
dysphoria/euphoria
zombie like state
tics or abnormal movement
HTN or pulse lfuctuations
hallucinations
reduce the dose, or change medication
Methylphenidate Products and important considerations
MPH IR
MPH ER
MPH ER CHEW
MPH CD
MPH LA
MPH XR SUSP.
MPH OROS
MPH MLR
MPH XR-ODT
MPH PM
MPH TRANSDERMAL PATCH
DEX-MPH IR
DEX MPH XR
MPH IR
onset:20-60 min
duration:3-6
doses per day: 2-3
pearls:–
MPH ER:
doses/day: 1
onset:60-80 min
duration: 3-8
pearls:–
MPH ER CHEW:
doses/day: 1
onset: 60-120
duration: 10-12
pearls: can be scored and halved
MPH CD:
doses/day: 1
onset: 20-60 min
duration:6-8
pearls: 30%IR and 70% XR. can be opened and put o n applesauce.
MPH LA
doses/day: 1
onset: 10-60 min
duration:6-8
pearls:50%ER and 50% IR. more beneficial for morning symptoms vs. CD because contains higher IR component.
MPH XR SUSP.
doses/day: 1
onset: 45 min
duration: 12
pearls: requires vigorous shaking for atleast 10 sec. must be reconstitiuted in phrmacy. good for 4 months after rec.
MPH OROS:
doses/day: 1
onset: 30-60 min
duration:10-12 hrs
pearls: SWALLOW WHOLE. PT WILL HAVE GHOST SHELL IN STOOL. not ideal for pt w. gi strictures because it wont breakdown and will comeout stool whole
MPH MLR:
doses/day: 1
onset: 20-60 min
duration: 12
pearls: beter for rebound afternoon symptoms due to larger ER dose
MPH XR-ODT:
doses/day:–
onset: 60
duration:12
pearls: dose 17.3 mg. not 1:1 conversion. need to retitrate when switching to this. do not chew or swallow whol. dissole on tongue, no liquid needed. dont push throug blister pack, peel.
MPH PM:
doses/day: 1
onset: >/=10 hrs
duration: 24-36
pearls: no more than 5% of ttoal drug absorbed in first 10 hrs. admin btw 630 and 930 pm. if dose missed, skip whle day and take following night at bedtime. 2 film hours
MPH transdermal patch
doses/day: 1
onset: 60-120 min
duration: 11-12
pearls: dose not eq. to oral. need to retitrate. drug active 3 hrs after removal. apply 2 hrs prior to desired onset. may be worn up to 9 hrs. can be worn while swimming and bathing. DO NOT CUT PATCHES. BBW: chemical leukoderma. can cause tics
Dex-MPH IR:
doses/day: 2-3
onset:30 min
duration:3-6
pearls: no greater benefit over MPH. 1/2 dose of MPH. cannot be changes 1:1
Dex-MPHXR
doses/day: 1
onset:30 min
duration:9-12
pearls: cannot be changed 1:1. 50%IR and 50%ER. afternoon symp. control not as good as OROS
DexMPH-SER-DEX-MPH: produg to DEX MPH
MPH specific conciderations
preffered product for children/ adolescents
inhibits reuptake of DA and NUE. DA» NE
titrate weeklyuntil clinical response is observed
time to peak can be delayed due to high fat meals
ramp effect: behavioral effects are prportional to rate of MPH aborption into cns
caution in pts w. tics, psychosis, and maoi use
safe in pts. w. epilepsy
priapism (prolonged erection of penis
Amphetamine Containing Products and considerations
MIXED AMP-IR salts
AMP S. IR
AM S. ODT,
AMP-XR SALT
AMPHETAMINE XR SOLUTION
AMP XR ODT:
AMP ER SUSP.
AMP XR
Mixed AMP -IR salts
doses/day:2-3
onset: 20-60min
duration:5-8 hrs
pearls: FDA approved in children >/3y.o
amphetamine sulfate IR
doses/day:1-2
onset:
duration: 4-6
pearls:FDA approved in children >/3 y.o
amphetamine sulfate ODT:
doses/day:1-2
onset:
duration:4-6
pearls:
mixed AMP-XR salts
doses/day:
onset:
duration:
pearls:50%IR,50%eR. MAY BE OPENED AND PUT ON APPLE SAUCE
amphetamine XR solution
doses/day: 1
onset:
duration:
pearls: not reconstitution. dose not 1:1 conversion. must retitrate. can cause epistaxis( nosebleeds) and allergic rhinitis
AMP XR-ODT
doses/day: 1
onset:
duration:10-12 HRS
pearls: can be taken w. or w.o food, but food can delay peak. do not chew. must be dissolves. no 1:1 conversion, does not need to be retitrated
AMP ER SUSP.
doses/day:
onset:
duration:10-12 hrs
pearls: can be taken w. or w.o food, but food can delay peak. do not chew. must be dissolves. no 1:1 conversion, does not need to be retitrated
d-AMP… IR, IR LIQUID, ER
lisdexamphetamine: designed for less abuse potential
amphetamine sulfate XR: has IR, intermediate release, and xr. no 1:1 conversion
amphetamine product considerations
preferred stimulant in adults
increase release DA and NE into resynaptic terminals
enhance release in NE peripheray
IR formulations given atleast bid, preffered for <5 y.o, afternoon dose should not be given < 6 hrs before bedtime
high fat delay time to peak
CI: pt hx of cv disease such as mod-severe htn, arrythmias, hf, RCENT MI
FDA APPROVED STIMULANTS in age groups..
> /=3
> /= 6
> /= 13
> /3:
AMP: IR amphetamines (adderal, evekeo, dextroamphetamine IR (dexedrine)
MPH: none FDA approved. HOWEVER, american college of pediatricts prefers PMH pver AMP products
> /6: can start using XR,
AMP:SR formulations. lisdexamphetamine (vyvanse), amphetamine ER( dyanavel xr, adzenys xr, adderall xr)
MPH: methylphenidate ir (ritalin), MPHER(ritalin sr) etc.
> /13: amphetamine/dextroamphetamine (mydayis)
Norepinephrine reuptake inhibitors
ex: atamoxetine ( (Strattera), Viloxazine ER (Qelbree)
mo: inhibit pre synpatic reuptake of NE
considerations: full benefit not seen until 6-8 weeks
atamoxetine: may require 2 doses in younger pts
viloxazine: youner pts may require a lower dose than adults
BBW:
atamoxetine: liver toxicity w. longterm use
both: depressants->new onset suicidality
AE: gi upset, psychiatric, qtc prolongation (not recommended in heart problems)
DDI: do not use incombo w. one another, qtc prolongation w. other QTC PROLONGATION APS, TCAs
amoxetine; incr. conc of paroxetine and fluoxetine
viloxazine: strong cyp12 inhibitor, weak 2d6 and 3a4 inhibitor
ADS: dulox., fluox.,parox,. venla, TCASs
APS: SGA
benzos
buprenorphine, hydrocodone, methadone, oxycodone
alpha adrenergic receptors agonists
clonidine ER (kapvay), Guanfacine ER(intuniv)
increase blood flow to prefrontal cortex ( enhances working memory and executive functioning) and inhibits NE release
AE:SEDATION!!! (clonidine), dizziness, hypotension, constipation, heart block
clonidine commonly added to stimulants. ER should not be taken w. high fat meal
other Trt. for ADHD
buproprion: weak dop. and ne reuptake inhibitor
adhd and dpression. less apetite supression and weightloss ocmpared to stimulants
TCAs: up to 4 weeks to see max effects
ae:sedation, constipation, overdose, heartbock, weightgain, rapid heart beat
Lithium/ anticonvulsants
effective for aggression, explosive behavior, impulsivity. childhood onset bipolar
APS: chlorpromazine and haloperidol for hyperactivity, impulsivity. neg. effects on learning, cognitive function, and can cause EPS
SGA: risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole. severe agression, risk of metabolic syndrome
general treament of adhd
preschool age children
*methylphenidate
school age children (6-11): mos well studied age group
adolesents(12-18)
geenral comorbidites cnsiderations
treat predom. symptoms first
adhd considered risk facor for development of substance abuse
*stimulant use does not affect risk of subsequent drug or alcohol abuse, later onset of stim. associated w. more substance use compared to if started earlier
oppositinal/ definant disorder w. adhd response to stimulant treatment
methylphenidate, clonidine, guanificine and atamoxetine reduce symptoms in children w. tics
patient evaluation for adhd after drug initiation
document baseline symptoms/complaints to evaluate imrpovement of drug intitiation
height, weight, eating, sleeping patterns, baseli.ne and q 3 months
atamoxetine, viloxazine, buproprion: adequate trial= 6 weeks at max tolerated dose
guanfacine/clonidine: monitor bp and pulse: adequate trial =1-2 months. ekg not mandatory, but often completed
