Week 7: ADHD, Neuro Pain

Question 1

Mechanisms of Pain

Answer 1

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

Question 2

CDC guideline for prescribing opioids for chronic pain

Answer 2

1. 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

Question 3

neuropathic pain .

Answer 3

Pain caused by a lesion or disease of the somatosensory nervous system.

neuropathic pain is a clniical description (NOT) a diagnosis

Question 4

characteristics of nervous system damage

Answer 4

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

Question 5

Presentation / assessment of neuro. pain

Answer 5

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

Question 6

neuropathic pain general treatment principles

Answer 6

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”

Question 7

NEUROPATHIC PAIN TREATMENT

Tricyclic AD(TCA’s)

examples:
advantages:
disadvantages
dosing

Answer 7

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

Question 8

NEUROPATHIC PAIN TREATMENT

SNRI

examples:
advantages:
disadvantages
dosing

Answer 8

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

Question 9

NEUROPATHIC PAIN TREATMENT

SNRI

Milnacipran (Savella)

Answer 9

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

Question 10

NEUROPATHIC PAIN TREATMENT

alpha 2 delta ligands

aka gabapentinoids

Answer 10

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

Question 11

NEUROPATHIC PAIN TREATMENT

Gabapentin

examples:
advantages:
disadvantages
dosing

Answer 11

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

Question 12

NEUROPATHIC PAIN TREATMENT

gabapentin products and dosing

Answer 12

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

Question 13

NEUROPATHIC PAIN TREATMENT

Pregablin

examples:
advantages:
disadvantages
dosing

Answer 13

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

Question 14

NEUROPATHIC PAIN TREATMENT
TRamadol

examples:
advantages:
disadvantages
dosing

Answer 14

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

Question 15

NEUROPATHIC PAIN TREATMENT

Tapentadol (Nucynta)

examples:
advantages:
disadvantages
dosing

Answer 15

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

Question 16

NEUROPATHIC PAIN TREATMENT

Capsaicin
examples:
advantages:
disadvantages
dosing

Answer 16

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

Question 17

NEUROPATHIC PAIN TREATMENT

available forms of Quetenza

Answer 17

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%)

Question 18

NEUROPATHIC PAIN TREATMENT
Lidocaine

indication:
onset:
duration:
dosing

Answer 18

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%)

Question 19

NEUROPATHIC PAIN TREATMENT

medical cannabis

Answer 19

studies found a “significant, but clinically small, reduction in mean numerical rating scale pain scores”

Question 20

Very general Tratment approach to neuropathic pain and considerations

Answer 20

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

Question 21

Painful Diabetic Neuropathy (PDN)

patho

Answer 21

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

Question 22

Painful Diabetic Neuropathy

tratment

Answer 22

1. increase NE and 5HT increase pain supression induced by the descending inhibitory pathways
2. TCAs
   also monoamine reuptake, nmda blockade and sodium channel interferance.
3. SNRI
   *duloxetine and venlafaxine

4.a2 delta ligands*gabapentin and pregablin

Question 23

General proposed treatment algorithm for PDN

Answer 23

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

3. if pain is still inadequately controlled
   *opioid agonist as monotherapy, followed by combo therapy if pai ncontroll is inadequatey

Question 24

Post herpetic neuralgia (PHN)

Answer 24

ractivation of varicella-zoster virus
(shingles)

distribution along dermatomes
ften causes PHN d/t sensory nerve damage, causing reduced neurite densities

Question 25

Treatment of PHN

Answer 25

1. 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

Question 26

Low Back Pain

Answer 26

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

Question 27

mangement of low back pain

Answer 27

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

Question 28

Fibromyalgia

Answer 28

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

Question 29

dx criteria of fibromyalgia

Answer 29

1. 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 3. symptoms havebeen generally presen for atleast 3 months 4. a dx of fibromyali is valid irrespective of other dx. a dx of fibromyalgia does not include the presence of other clinically importnt illnesses

Question 30

pharm treatment of fibromyalgia

Answer 30

amitryptiline (at low dose) duloxetine or milnacipran(can also relieve fibromyalgia fog) prgablin cyclobenzaprine

Question 31

comprehensive algorithm for the pharm management of neuropathic pain

Answer 31

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

Question 32

Risks and prognostic factors of ADHD

Answer 32

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

Question 33

Patho of ADHD

Answer 33

1. cortical thinning and delay in cortical thickness, causing reduced activity in prefrontal and anterior cingulate cortex. 2.default mode network over-activity.. and others

Question 34

SS of ADHD

Answer 34

inattention: wandering off tasks, lacking persistence, having difficulty sustaining focus, being disorganized 2. hyperactivity: excessive motor activity, fidgeting, tapping, talkativeness, extreme restlenessness 3. impulsivity desire for immediate rewards or inability to delay gratification social intrusiveness, making important decisions without considerations of long term consequences

Question 35

differential dx fADHD

Answer 35

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

Question 36

ADHD dx

Answer 36

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

Question 37

dx of inattention / hyperactivity (impulsivity)

Answer 37

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

Question 38

presentation types of ADHD

Answer 38

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

Question 39

presentation of ADHD in adults

Answer 39

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

Question 40

presentation of ADHD in school age children (age 6-11)

Answer 40

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

Question 41

functional consequences of adhd

Answer 41

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

Question 42

Non pharm treatment of adhd based on age gorup

Answer 42

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

Question 43

general treatment principle for trt of ADHD

Answer 43

COMBO NON PHARM AND STIMULANTS HAVE greater improvements in academic/ conduct measures tan either intervention alone

Question 44

General trt algorithm for ADHD if pt is predom ADHD presenting

Answer 44

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

Question 45

General trt algorithm for ADHD if pt has predom. comorbid presenting symptoms

Answer 45

1. 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 2. 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 3. anxiety or depression a.treatment: Antidepressant b.some response: add stimulant c.inadequate response: alternative antidepressant

Question 46

pearl for comorbid ADHD and bipolar treatment

Answer 46

ALWAYS MANAGE BIPOLAR DISORDER FIRST RISK OF INDUCING MANIC OR HYPOANIC EPISODE W. treatment of stimulants or atomoxetine or viloxazine in uncontrolled BPD

Question 47

Stimulant considerations

Answer 47

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

Question 48

stimulants moa GENERAL DOSING AE: DDI

Answer 48

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

Question 49

adverse effect management of stimulants 1.reduced appetite/weightloss 2. stomach ache 3. insomnia 4. headache 5. rebound symptoms 6.inrritiability / jitteriness

Answer 49

1.reduced appetite/weightloss: high calorie meals when stimulant effect is low (breakfast/bedtime) cyproheptadine @bedtime 2. stomach ache: take on full stomach, lower dose 3. insomnia: give dose earliler in the day, lower last dose of day/ give earlier, add sedating meds @hs (guafenicine, clonidine, melatonin, or cyproheptadine 4. headache; divide dose, give w. food, or gve an analgesic 5. rebound symptoms: long acting stimulant, atomoxetine, antidepressent 6.inrritiability / jitteriness: assess for comorbid condition, reduce dose, consider mood stanilizer or atypical APS

Question 50

uncommon stimulant side efects and what to do

Answer 50

dysphoria/euphoria zombie like state tics or abnormal movement HTN or pulse lfuctuations hallucinations reduce the dose, or change medication

Question 51

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

Answer 51

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

Question 52

MPH specific conciderations

Answer 52

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

Question 53

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

Answer 53

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

Question 54

amphetamine product considerations

Answer 54

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

Question 55

FDA APPROVED STIMULANTS in age groups.. >/=3 >/= 6 >/= 13

Answer 55

>/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)

Question 56

Norepinephrine reuptake inhibitors

Answer 56

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

Question 57

alpha adrenergic receptors agonists

Answer 57

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

Question 58

other Trt. for ADHD

Answer 58

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

Question 59

general treament of adhd

Answer 59

preschool age children *methylphenidate school age children (6-11): mos well studied age group adolesents(12-18)

Question 60

geenral comorbidites cnsiderations

Answer 60

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

Question 61

patient evaluation for adhd after drug initiation

Answer 61

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