Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

TPX Neuro, Psych, & Sub abuse > Week 6: Stroke, Sleep > Flashcards

Week 6: Stroke, Sleep Flashcards

1
Q

What is a Transient Ischemic Attack (TIA)

A

cerbral ischemic event lasting less than 24 hours (typically only minutes without apparent parmanent neurologic deficit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Completed Stroke-

A

cerebral ischemic acute event with deficit that persists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Other types of ischemic strokes

a)Hemispheric Infarct
b)Lacunar Infarct
c)Microvascular Ischemic White Matter Lesions

A

a) stroke, usually caused by occlusions of carotid artery, leading to infarct of entire hemispheres of the brain. can be

b) blockage of arteries that supply deeper portions of the brain

c) occlusion of very small blood vessels in white matter. Pts. often times can be asymptomatic. treatment is controversial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatable Risk factors for Stroke

A

HTN

hypercholesterolemia

heart disease (espatrial fibrillation)

DM

cigarette smoking

excessive alcohol intake

phsyical inactivity

obesity

carotid bruit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Untreatable risk factors for stroke

A

age

sex

race

prior stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

stroke pathophysiology

A

thrombus formation
1. asymptomatic atherosclerotic plaque

  1. platelet deposition
  2. occlusive thrombus formation
  3. plaque fissure-> red thrombus->embolism
    a.primary hemostasis-platelet plug
    b-coagulation->fibrin clot->thrombus

cardiogenic embolus-blood stasis->thrombus->ejected to brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical presentation of stroke/TIA

Carotid territory

A

unilateral weakness

unilateral sensory symptoms

aphasia- difficulty understanding peech or speaking, or both

monocular visual loss

transient global amnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical presentation of stroke/TIA

vertebrobasilar territory

A

bilateral weakness, sensory, and/or visual complaints

  1. diplopia, ertigo, ataxia w.o weakness, dysphagia (difficulty swallowing)

hard to distinguaish a vertebrobasilar stroke from other differential diagnosis. one distinguishing factor is the rapidity of symptoms for a vertebrovascular stoke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

General SS of stroke

A

unilateral weakness
unilateral sensory symtpms

dysphasia

dysarthria (slurred speech)

vision disturbances

sudden confusion/mental status changes

facia droop

seizures (rare)

ataxia

loss of balance

verigo

dizziness

dysphagia

headache

vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phases of stroke care

A

Primary prevention

acute management of stroke

secondary prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

primary prevention of stroke

A

modifiable risk factors
a. HTN, HLD, smoking, DM, a. fib, cad, obesity, post menopausal hormone therapy

nonmodiafiable risk factors:
a.age>55, race (black,hispanic), male gender, family hx of stroke/TIA, personal hx of stroke/tia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who are at highest risk for having a stroke

A

patients who have had a previous stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

General Treatment of an intial cerebrovacular event

A

ANTIPLATELET THERAPY
*small vessel lacunar
*Large Vessel Embolic
*Large Vessel thrombotic

WARFARIN THERAPY
Cardioembolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

General Platelet cascade in thrombus formation

A

fissure in lipid plaque recongnized by the body as injury activates platelets, adhere to fissure, followed by platelet aggregation on fissure.

recruit fibrin and RBC, causing a clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of Action of Anti-platelet Agents

A

a)Ticlopidine/Clopidogrel/ Praugrel: IRREVERSIBLY Block ADP receptors, inhibiting platelet aggregation

b)Aspirin: IRREVERSIBLY inhibits COX enxyme and thromboxane(potent activcator of platelet aggregation), leading to inhibition of platelets

c) Dipyridamole: REVERSIBLY increases plasma adenosine and inhibits platelet phosphodiesterase, causing inhibition of platelet activation and aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Secondary stroke ppx

A

ASA
Ticlopidine
Clopidogrel
Prasugrel
Ticagrelor
ASA/ER dipyrdamole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Notes on PK of aspirin

A

~18-25% decreased risk of having another stroke

  • inhibition of plt. aggregation require ~97% of COX-1 inhibition

*in ~70% of pts. this is achieved with an aspirin dose of 80-100 mg

*older age and obese patient may require higher doses of aspirin to produce effect

*inhibition of thromboxane occurs pre-systemically in portal circulation

*enteric coated products are erratically absorbed from the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ticlopidine vs. Aspirin

A

additional 21% risk reduction of having another stroke in comparison to aspirin

fatal toxicity risks, including diarrhea, rash, nausea, and gastritis, ulcer, GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clopidogrel vs Aspirin

A

CAPRIE study shows that clopidogrel has ~7% additional risk reduction of having another stroke, which is not statistically significant.

only statisticlaly significant finding from CAPRIE study was that clopidogrel had 23.8% relative risk reduction of PAD over aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dipyridamole ER vs. Aspirin

A

Dipyridamole ER (which has ~ same RRR as aspirin) not available in the US, only IR

ESPS2 study showed that inorder to achieve same time conc. of Dipyridamole ER with IR, pt must take IR 100 mg QID for the rest of their life, which would drastically increase risk of pt noncompliance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Aggrenox vs. Aspirin

A

Aggrenox is Dipyridamole ER+ASA combo

ESPS 2 study showed 36.8% RRR vs placebo and 23% RRR vs ASA.

HOWEVER, PROFESS study showed there is no difference btw. aggrenox and clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Overall, how to pick an antiplatelet agent best for the patient

A

Since there are no significant differences btw. anti-plt. choices, anti-plt agents used is based on whats best for individual patient.

A)base it on pt specific needs

consider..
side effect profile relative to your pts hx
(ex. Aggrenox can cause vascular headache, can cause GI problems->caution in GI problems..etc.)

the agent that produces an inhibition of aggregation in your specific patients (ex: some pts can be aspirin reisstant due to genetics)

can be used in lowest effective dose to reduce risk of bleeds

b) will aparticular agent be less than optimal for a particulr pt
*ex: ASA allergy
*pts on clopidogrel may have DDI w. agents that inhbit CYP2C19 such as CCBs, PPI’s etc.
*aggrenox therapy andmigraine hx
*aggrenox therapy and spastic colon or IBS

c)does your patient warrent dual anti-plt therapy
*Clopidogrel + ASA only has increased anti-plt effects in firt 30-90 days, then risk of bleeding outweighs beenfit
*coronary artery stenrs and new cerbral ischemia
*a. fib not able to take coumadin

d) are your pt plt. responding to their anti-plt agent
*ex: ASA or Plavix resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Individualized pharmacotherapy for anti-plt. choice

A

urgency of needing full antiplt. therapy

agent least likely o produce adverse effects
*headache hx
*spastic coloitis or ulcerative colitis/chrons
*gastric ulcer hx
*true aspirin alergy

agent least likely for drug interactions
*need for chronic NSAID, PPI, or CCB use

dual anti-plt therapy
*failure of monotherpay
*first 3-6 mo post troke w. high risk factors
*a. fib w. CI for anticoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

approach to ASA resistance

A

assurance compliance
*urinary salicyates

remove drugs that compromise ASA effects
*NSAIDS other than celecoxib(celebrex)
*some herbal supplements

change from EC to chewable ASA or alka seltzer
*particularly in older women

*change ASA dose where appropriate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

approach to plavix resistace

A

minimize use of other drugs that inhibit cyp3a4 AND CYP2C19

SUBSTITUTE DRUGS THAT HAVE LESSOR EFFECT ON THESE p450 is iso enzymes

add meds that can induce CYP enzyme activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

common meds that influence CYP3A4 or CYP2C19

A

statins other than Rosuvastatin (crestor)

CCBs, not BB, ACE, or ARBS
*NOTE: IF CCB + clopidogrel is an issue in a pt, before switching the CCB, be sure pt is on CCB for htn and not rate control. if ccb used for rate control is changed, might do more harm in pt.

Ambien, Lunesto (Sonata least likely)

Gliburide, not glipizide or metformin

Enablex, Ditropan, not detrol or sanctura

PPI’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what to do if pt is truly resistant to both aspirin and clopidogrel

A
  • ticagrelor

*prasugrel

BOTH OF THESE NOT FDA approved.

*max ASA dose 100 mg daily w. ticagrelor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Signs and symptoms of sleep disorders

A

excessive daytime sleepiness (EDS)

impaired daytime funcitoning

irregular breathing

increased movement during sleep

irregular sleep and wake cycle

difficulty falling asleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

common types of sleep disorders

A

insomnia

sleepapnea

narcolepsy

circadian rhythm disorders

parasomnia

restless leg syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is insomnia

A

most common reported sleep disorder

difficulty falling asleep, maintaining sleep, or non restorative sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

categories of insomnia

A

transient insomnia: several days

<3 months: short-term insomnia

atleast 3 nights per week for >/=3 mo.: chronic insmonia

32
Q

causes of transient insomnia

A

stress

jet ag or shift work

schedule change

medical (chornic pain0

psychiatric (eg. anxiety, PTSD)

pregnancy

pharm. induced

33
Q

causes of short term (<3 mo.) insomnia

A

untreated or undertreated transient insomnia

acquired exacerbating behavior

34
Q

common drrugs that can cause or worsen insomnia

A

alcohol, caffeine, nicotine

anticholinergics

SSRISNRIs

alpha blockers

beta blockers

ACE and ARBS

cholinesterase inhibitors

bronchodilators

CNS stimulants

corticosterois

decongestants

diuretics

H2RAs

statins

opioids

35
Q

treatment goals for transient insomnia

A

orrect ynderlying sleep complaint, avoid AE of meds

treatment: adequate bedtime doses of benzos for 2-3 weeks

selection of specific med is patient dependent:

*desirability for daytime anxiolytics
*need fo rnext day early morningcognitive sharpness
*interactions with other medications
*d/c of problematic meds
*pk profile of the BZDRA and specific insomnia complaints

36
Q

tratment of short term insomnia goal

A

a treatment plan that will result in the pt sleeping normally w. no medications

37
Q

non pharm treatment of insomnia

A

maintaine a regula sleep schedule

establish a calm bedroom setting (quiet room, no bright lights, comfortable temp/)

do not spend time in bed if awake
imit intake of nicotine, caffeine, and alcohol

exercise regulalrly but not close to bedtime

have a light snack or warm bevarage befor ebedtime

avoid watching the clock, remove bedroom clock if necessary

38
Q

treatment oflongterm insomnia

A

proper dx of root/psychiatric cause of insomnia

CBT for insomnia
*preffered 1st line therapy for chronic insomnia in mos patients
*CBT-I+/- meds> meds alone

if rapid improvement is necessary, can use CBT-I_ meds initially w. plan to taper medication over time

39
Q

Treatment options for insomnia

BZDRAs

A

most commonly used trt. for insomnia

fda approved for insomnia

labels include a cuation for anaphylaxis, facial angioedema, and complex sleep behaviors

agonist effects on gaba receptors

includes newer non-benzo GABA agonists and traditional benzos

always ake before bedtime

use w. caution in elderly

drowsiness, dizziness, confusion, risk of falls

avoid w.alcohol

withdrawal symptoms upon abrupt d/c i.e termors, muscle cramps, seizures

40
Q

considerations for BZDRAs

benzo hypnotics

A

CHOICE OF A PARTICULAR BZDRA IS BASED ON PK PROFILE AND PT. PRESENTATION

reduce sleep larency

increased stage 2 sleep and decrease delta sleep

anxiolytic effect

so not use in pts w. sleep apnea or substance abuse

avoid alcohol and cns depressants

side effects are dose dependent

BBW: concaminant use with opioids can cause resp. depression,sedation, coma, and death

*increased risk of abuse, misuse, and addiction

*continued use can lead to clinically significant physical dependence

41
Q

considerations for BZDRAs

Non benzo GABA agonists

A

CHOICE OF A PARTICULAR BZDRA IS BASED ON PK PROFILE AND PT. PRESENTATION

“Z” drugs

more selective

increase total sleep time

less disruptive of sleep stages

geenrally have less withdrawls. tolerance, and rebound insomnia

associated w. parasomnic episodes w. amnesia

BBW: can cause complex sleep behaviors(i.e sleep walking, sleep driving, and engaging in other activities while now fully awake. d/c immediately if develops.

42
Q

Estazolam

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule: CIV

Benzo vs Z drug: Benzo
Indication: sleep onset or maintenance. short term mgt of insomnia characterized by difficuly in falling asleep, frequent nocturnal awakenings, or/or early morning awakenings

PK(t1/2 &tmax):
*tmax:2
t1/2: 10-24 hrs

AE: hypokinesia

considerations:
CI in pregnancy or w. itroconazole or ketoconazole

43
Q

Eszopiclone (Lunesta)

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule: CIV

Benzo vs Z drug: Z drug

Indication: sleep maintenance or early morning awakenings

PK(t1/2 &tmax):
t1/2: 1 hr
tmax: 6 hr (up to 9 in elderly

AE: headaches, dysgeusia, nervousness/anxiety, xerostomia, infection, upset stomach

considerations:
*rapid absorption tat can be delyed w. food
*can be used long term fo rup to 6 months
*major cyp3a4 substrate
*monitor w. concurrent use of cyp3a4 inhibitors (keto, itraconazole)

44
Q

Zaleplon (Sonata)

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule: cIV

Benzo vs Z drug: Z drug

Indication: short term trt of insomnia. does not reduce nighttime awakening

PK(t1/2 &tmax):
t1/2: 1 hr: could be delayed w. absorption
tmax: 1 hr

AE: headache, nausea, abdominal pain

considerations:
*cyp3a4 substrate
ultra short acting, rapid onset
avoid taking after a highfat meal delays absorption
short term treatment

45
Q

Zolpidem

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:CIV

Benzo vs Z drug: Z drug

Indication: depends on formulation
IR tablet or spray: sleep onset. off label for sleep maintenance
ER tablet: sleep onset or maintenance
SL tablet: dif. dose based on sex: take if more than 4 hours remain before waking and pt has trouble returning to sleep

PK(t1/2 &tmax):
t1/2: 0.6-4hrs
tmax:1.4-8.4 hrs

AE:headache and nausea, increased hypotension and falls in elderly

considerations:
avoid use in severe hepatic impairment

minimal tolerance and rebound at recommended doses

diff formulations have diff indications

46
Q

Trazadone

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:–

Benzo vs Z drug:–

Indication: offlabel use for sleep continuity

PK(t1/2 &tmax):

AE: caryover sedation, alpha adrenergic blockade(orthostasis) priapism is a rare side effect

considerations:
usefel in pts. w. hx of substance abuse and or depression

when d/c taper dose over 2-4 weeks

BBW: suicidal thoughts and behaviors, same risks as antidepressants

47
Q

first gen antihistamines

Schedule:

Benzo vs Z drug:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:–

Benzo vs Z drug:–

Indication: OTC option for mild insomnia

PK(t1/2 &tmax):–

AE: anticholinergics

considerations:
avoid in elderly
tolerance to sedative effects develop quickly

48
Q

Suvorexant (Belsmora)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:CIV

Benzo vs Z drug:–
*dual orexin A and orexin B antagonist (DORA)

Indication:sleep onset and maintening sleep by wurning off wake signaling

PK(t1/2 &tmax):
t1/2: 12 hrs
onset: <30 min

AE: DROWSINESS, dizziness, headache, sleep paralysis, abnormal dreams, URTI

considerations:
interactions w. cym3a4 inhibitors
decrease dose w. mod. cyp3a4 inhibitors, CI w. strong 3a4 inhibitors
CI in narcolepsy

49
Q

Lemborexant (Dayvigo)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:CIV

MOA: Dual Orexin A and Orexin B receptor antagonist (DORA)

Indication: assists in getting to and maintainning sleep, turns off wake signaling

PK(t1/2 &tmax):
Onset:<30 min
t1/2: 17-19 hours

AE: drowsiness, dizziness, headache, complex sleep behaviors, abnormal dreams (nightmares)

considerations:
*decrease dose w. weak CYP3A4 inhibitors
8not recommend w. strong cyp3a4 inhibitors
CI in narcolepsy
*take at bedtime w. atleast 7 hrs beforeplanned time of awakening

50
Q

Ramelteon (Rozeram)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:– not controled

MOA:meletonin receptor agonis selective for MT1(induces sleep) MT2 (regulates circadian rhythm) (MT1>MT2)

Indication: isleep onset insomnia and for long term use

PK(t1/2 &tmax):
onset: 30 min
t1/2: 1-2.6 hrs

AE: headahce, dizziness, somnelance

considerations:
do not use in pts w. liver disease
not controlled
not as effective in pts who have beent reated already with a BZDRA

CI: w. fluvoxamine

51
Q

Melatonin

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:– Dietary supplement not fda approved

MOA:

Indication: beneficial effects on sleep latency, shift workers, and jet lags

PK(t1/2 &tmax):–

AE:-

considerations:
should not be used in pts w. autoimmune conditions on immune modulators and has been shown to alleviate some autoimmune conditions but exacerbate others

less effectin pts whove used bzdraS

52
Q

Doxepin

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Schedule:–

MOA: INHIBITS REUPTAKE OF SERETONIN AND NOREPINEPHRINE ANTAGONIZES h1 HISTAMINE RECEPTOR

Indication: sleep maintenance insomnia

PK(t1/2 &tmax):

AE:

considerations:
lower than dose used for depression is used for sleep

BBW for suicidality in pts <24 years
do not tak w. in 3 hrs of a meal due to slower absoprtion

53
Q

Considerations for pharmacotherapy for elderly and pregnant women

A

non pharm preffered initially, if oharm therapy is needed…

Elderly
*CBT-I
*Ramelteon
*Eszopiclone
*Zolpidem
*low dose doxepin

Pregnancy
*diphenhydramine
*Doxylamine
*low dose doxepin

54
Q

Sleep apnea

what is it

A

repeated episodes of cessation of breathing during sleep, followed by blood oxygen desaturation and arousal from sleep to restart breathing

fragmented sleep and poor sleep architecture w.periodsof apnea and hypopnea

55
Q

TYpes of sleep apnea

A

Dx w. polysomnography
*Central (csa): impairment of resp. drive

Obstructive(OSA): upper airway collapse and obstruction

Mixed: CSA and OSA

56
Q

CHaracteristics of Obstructive slepe apnea

A

multiple episodes of airway closure and cessation of breathing per hour

can be caused by obesity, narrow airway, or other anatomical factors

multiple awakenings and arousals perr hour w. apneas, gasping or both throughout the night

significant o2 desaturations per hour

associated w. MVA, depresison, increased cancer risk, stroke, and cva

linked to CV AND cerebrovascular morbidity

increased risk for drug resistant htn

57
Q

treatment of sleep apnea

A

first line: standard of trt is nasal positive airway pressure during sleep through a cpap

Weight management

avoid all cns depressants (such as benzos or opioids) and drugs that can cuase weight gain. use extreme caution in apioid medications

if cpap doesnt work, can use medication for excessive daytime sleepiness

58
Q

Narcolepsy

what is it

A

severly debiliating neurologic disease, oftenundiagnosed

impairment of both oncet and offset of rem AND NREM

59
Q

narcolepsy tetrad

A

excessive daytime sleepiness, cataplexy, hallucinations, sleep paralysis

patho: loss of normal funciton of hypocretin orexin neurotransmitter system possibly due to autoimmune process

60
Q

Narcolepsy treatment

nonpharm
pharm

A

non pharm: good sleep hygeine and scheduled daytime naps

avoid drugs that can worsen daytime sleepiness (benzos, opiates, aps, ALCOHOL)

pharm: focus on treatment of excessive daytime sleepiness (EDS)
*modafanil or armodanil trt for eds
*tca’s, snris, ssris

61
Q

Medications EDS in narcolepsy

Modafinil

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Medications EDS in narcolepsy

Schedule: C-IV

MOA: unclear, effects on dopamine, GABA, 5HT

Indication: EDS in narcolepsy

PK(t1/2 &tmax):

AE: headache, nausea, anxiety/nervousness, dizziness, dyspepsia, xerostomia, back pain, rhinitis

considerations:
Avoid use in regnancy
may decrease effectiveness of contraceptives (cyp3a4 INDUCERS)
use caution in pts. w. CV disease, esp not recommended in pts. w. left ventricular hypotrophy

62
Q

Medications EDS in narcolepsy

Amodafinil (Nuvigil)
Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Medications EDS in narcolepsy

Schedule: c-iv

MOA: r-enantiomer of modafinil, moa unclear

Indication: EDS in narcolepsy

PK(t1/2 &tmax):

AE: headache, insomnia, dizziness, nausea, xerostomia

considerations:
avoid use in pregnancy
may decrease effectiveness of contraceptives (CYP3A4 inducers)
use in caution in pts. w. cv diease, esp not recommended in pts w. a history of left ventricular hypertrophy

63
Q

Medications EDS in narcolepsy

Solriamfetol (Sunosi)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Medications EDS in narcolepsy

Schedule: C-IV

MOA: dopamine and norepinehrine reuptake inhibitor

Indication: EDS in narcolepsy

PK(t1/2 &tmax):

AE: headache, anxiety, insomnia, decreased appeptite nausea

considerations:
CI w. MAOI, do not use concurrently or w.i 14 days of MAOi

64
Q

Medications EDS in narcolepsy

Pitolisant ( Wakix)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Medications EDS in narcolepsy

Schedule:–

MOA:antagonist/ inverse agonist at histmaine 3 rceptors

Indication: EDS in narcolepsy

PK(t1/2 &tmax):

AE:headahce, anxiety, musculoskeletal pain, uri

considerations:LOWER MDD FOR KNOWN CYP2D6 METABOLIZERS
MAJOR CYP2D AND CYP3A4 INTERACTIONS
CI IN SEVERE HEPATIC IMPAIRMENT

65
Q

Medications EDS in narcolepsy

Sodium Oxylate (Xyrem)

Schedule:

MOA:

Indication:

PK(t1/2 &tmax):

AE:

considerations:

A

Medications EDS in narcolepsy

Schedule: C-III

MOA: cns DEPRESSANT. GABAb receptor activity at noradrenergic and dopaminergic neurons

Indication:

PK(t1/2 &tmax):

AE: ocnfusion, headache, dizzeness, weightloss/decreased appetite, urinary incontinance, drowsiness, depression, somnambulism, anxiety

considerations:
BBW: cns depression, abuse/misuse, restricted access.

can only be obtained thruogh a REMS program
*even tho a cns depressant, improves pt sleep so they are more well rested the next day

dosed at bedtime after pt is in bed w. second dose 2.5-4 hrs later

66
Q

List of meds used in cataplexy in narcolepsy

A

cataplexy (sudden loss of muscle tone)

REM SUPRESSING DRUGS
*Fluoxetine (SSRI)
Venlafaxine (SNRI)
Atomoxetine (SNRI)
Clopiramine (TCA)
Imipiramine (TCA)
Nortriptaline (TCA)

PITOLISANT

SODIUM OXYBATE

67
Q

Circadian Rhythm Disorders presentation

A

presents as either insomnia or hypersomnia

commonly manifest as jet lag or shift work disorder

68
Q

Jet lag treatment

non pharm
pharm

A

non pharm
*napping (<30 min in length atleast 8 hrs before bedtime)

times light exposure

pharm :
Meletonin
ramelteon
short acting BXDRA- risk for next day drowsiness

takrdrug at target destination bedtimes to reduce jetlag and shorten sleep latency

69
Q

Shift work disorder

A

difficulty . sleep or wakefuleness at times that are imposed by shifts running counter to the light dark schedule

non pharm:
sleep scheduling
sleep hygeine
naps before or during shift if possible
esposure to bright lights at night and darkness during the day

pharm:
meletonin (0.5-5)
ramelteon
short acting bzdra. BE CAREFUL for risk of next day drowsiness
modafinil and armodafinil to improve wakefulness

70
Q

Parasomnias

A

abnormal behavior or physiological events that occur during sleep such as

sleep walking, sleep driving, sleep terrors, sleep talking, nightmares, etc.

sleep walking terrors and talking during NREM sleep

may be due to a z drug w. alcohol or antidepressants

71
Q

treatment of parasomniaas

A

protect the individual fromharm: safety latches on doors/ windows

BZ, ssri, OR TCAs may be beneficial

reduce stress, anxiety, and sleep deprivation to reduce nightmares

72
Q

Restless leg syndrome

A

parasthesias felt deep in the calf muscles, thighs, and arms w. an urge to keep limbs in motion; often bilateral

associated w. ckd, iron defiicnecy, vit. b or folate defiiciency, pregnancy, peripheral neuropathies

73
Q

Rule out/ Treat Possible Causes of RLS

A

nutrition: iron supplementatino with Fe deficiency

vit. B or folate deficiency

reduce caffeine and alcohol use

wieghtloss

smoking cessation

regular moderate exercise

sleep

withdraeal of meds which may cause RLA
*centrally acting antihistamines (diphenhydramine, doxylamine, hydroxyzine, meclizine)

AD(TCA’S SSRI, SNRI)(NOT buproprion)
APS
antinausea drugs that block dopamine (metoclopramide, promethazine)

74
Q

non pharm treatment of RLS

A

treatment factors:
age of pt
severity, duration, and frequency of SS
comorbidities

SS releif: walking, biking, soaking limbs, leg massage

activities to improve mental alertness at time of rest/boredom

yoga or acupuncture?

75
Q

pharm trt for RLS

A

intermittent symptoms; carbidopa-levadopa
BZDRA: clonazepam most well studied

chronic and persistent symptoms:
Alpha-2delt calcium ligands
*pregablin
*gabapentin
dopamine agonists
*immediate-release pramipexole
Ropinirole
*rotigotine

76
Q

considerations for specific classes of drugs for rls TREATMENT

A

dop. agonists
*use lower doses compared to PD treatment
augmentation is problematic, can cause increase in rls

BZDRAS
cautin: caryover sedation

Alpha-2delt calcium ligands
good choice for painful RLS
gabapentin enacaribl 9Horizant) is FDA approved for RLS

TPX Neuro, Psych, & Sub abuse (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions