Key Points Quiz 3

Alzheimer’s is due to

low levels of Ach in brain

-Ach=excitatory

early-moderate stages AD use

Aricept (Cholinesterase inhibitor)

-prevents breakdown Ach

-SE: N/V, diarrhea, WL, muscle weakness, generalized pain, fatigue, dizziness, insomnia

-AE: symptomatic bradycardia, syncopal episodes, fall

***increased fall risk!

moderate-severse stages AD use

Namenda (NMDA antagonsit)

-blocks glutamate in brain

-unsown if more effective but better tolerated

-SE: HA, constipation, confusion, dizziness

**Ensure fall and seizure precautions!

ensure ____ precautions for Namenda and Aricept

fall and seizure

MS due to…

Chronic, inflammatory autoimmune that damages myelin sheaths in CNS

drugs for MS do what?

-Signs and Symptoms: spasms, spasticity, incontinence, depression, neuropathic pain

^***know pt take variety of drugs depending on symptoms they have

SE MS drugs: Inferferons

-all: injection site reactions

-others: flu-like reactions; liver injury

if MS acute relaspe, might use

-steroids/IV glucorticoids

-IV gama gobulin

MS Therapy implications

-PT most beneficial when it coincides with pharmacotherapy

-Fall prevention: balance training and home safety assessments

excitatory or inhibitory?

-Ach

-GABA

-Glutamate

-excitatory

-inhibitory

-excitatory

Benzodiazepines: SE and AE

-SE: sedation, psychomotor slowing

-AE: respiratory depression (when used w/ other CNS depressants), abuse potential (schedule IV), drowsiness, anterograde amnesia

Benzodiazepines: therapy implications

-no ETOH, heavy machinery, or long-distance driving

-concern=tolerance/dependency/withdrawal

• avoid long-term use/taper dose

-falls in elderly

Nonbenzodizepines: SE and AE

-SE: GI discomfort, dry mouth, sore throat, muscular incoordination, CV and respiratory depression

-Complex behaviors: sleep walking, drive or eat while sleep -> occurs with no memory of activity, more likely if high dose or w/ alcohol

Nonbenzodizepines: PK

metabolized in liver; can be stored in adipose tissue -> slowly leak out into CNS causing sedation/hangover

anti-anxiety drugs decrease anxiety as the expense of…

sedation -> are NOT curative -> intended to be short term while pt develops more effective management techniques

true or false: anti-anxiety drugs (Buspirone) have fewer side effects and lower risk of dependence than benzodiazpeins?

true!

-and also increases effects seretonin in brain

anti-anxiety: therapy implications

-sedation -> risk for falls, decreased participation

depression due to…

decreased levels of amine NT: norepinephrine, dopamine, and serotonin in the brian

depression drugs can help with…

chronic pain and depression

depression TCA: uses + SE/AE

-Use: depression, neuropathic pain, fibromyalgia, post-herpetic neuralgia

-SE: hypotension (esp elderly), drowsiness, sedation, significant anticholinergic effects

-AE: cardiac toxicity-ventricular arrhythmias, QT prolongation, AV block

depression MAOI: SE + AE

-SE: drowsiness, dizziness, HA, nausea, xerostomina

-AE: hypertensive crisis (MI and CVA), seizures

• CNS excitation: restlessness, irritability agitation sleep loss

• Anticholinergic effects

• Increased BP

MAOI can interact w/ what food?

-tyramine food (fermented foods and wines, aged cheese, etc.)

what med has a black box warning for suicidal ideation/plans (<24 years)?

SSRI

which meds can cause serotonin syndrome?

-SSRI

-SNRI (<SSRI)

-Alpha 2 Agonist

SSRI: SE

-SE: GI complaints (N/V/D), insomnia, restlessness, HA, sexual dysfunction

-Serotonin Syndrome: black box warning=suicidal ideation/plans (<24 years)

*increases synaptic serotonin

NDRI: AE

-increased risk of seizures due to lowering seizure thresholds

Alpha 2 antagonist: AE

-serotonin syndrome, agrandlocytosis, neutropenia

Bipolar: 2 key takeaways

-Lithium (AE=toxicity due to accumulation)

-pt w/ bipolar may be on multiple medications leading to multiplied SE

therapy implications: depression and bipolar

-Schedule sessions when drugs effective (4-6 weeks)

-Associated w/ falls in older adults

-Promote nonpharmacological treatment

-Asses for signs and symptoms of anxiety/depression/suicide

-Know SE (sedation and hypotension) and AE (serotonin syndrome and hypertensive crisis)

seizure: key takeaways

-Irriation of the brain

-2 Dif types of seizures: generalized and local; Need to determine type of seizure to determine drug

-Regular bloodwork to ensure therapeutic level

-Newer drugs better than traditional, safer and better tolerates

seizure: 1st generation

-Barbiturates: limited bc strong sedation and other AE, small therapeutic index and potential OD

-Hydantonins-Phentoin: Dilantin first drug used for epilepsy

-AE=include rashes

seizure: 2nd generation

-NOT more effective than 1st generation but have relatively mild side effects

-Gabapentin: also treats chronic and neuropathic pain

-Pregabalin (Lyrica)

seizure: therapy implications

-History and effectiveness

-May need to treat SE like ataxia (use a device for?)

-Rashes, so modify to don’t irritate skin

-Alter environment to decrease triggers: lights, sounds

-AE: sedation, dizziness, ataxia, gastric disturbances, changes in behavior or function

psychosis: therapy implications

-pt will have a better disposition during therapy

-Monitor for movement and nonmovement SE

• Movement: tardive dyskinesia, pseudoparkionism, akatshia, dyskinesia, neurleptic maligant syndrom

• nonmotor: sedation, antichol SE, hypotension, photosensativity

-check for orthostatic BP/hypotension

Parkinson’s is due to

decreased levels dopamin

Levodopa/Sinemet/Cardiopa: MOA

-Brain needs dopamine, but dopamine cannot cross BBB -> levodopa can cross BBB -> once in brain converted to dopamine by enzyme decarboxylase and then activates dopamine receptors

• Can be metabolized before brain, so add Cardiopa to prevent breakdown

Levodopa/Sinemet/Cardiopa: SE and AE

-SE: N/V, dyskinesia, CV (arrhythmias, hypotension), psychosis

-AE: freezing

what food avoid w/ Sinemet?

high-protein meals reduce therapeutic response

end of dose akinesia=

-”wearing off” develops near end of dose; ”on-off” phenomenon

-do treatment when working

anticholerngics SE

”can’t pee, see, spit, shit”

-urinary retention, pupillary dilation, decrease secretions, decrease bowel movements

Parkinson’s: therapy implications

-PT most beneficial when w/ meds

-schedule therapy around “on-off” times

-high protein diets can impact

-fall prevention and balance training is paramount

-home safety assessments to decrease fall risk

-interdisciplinary communication

what stage want to get to with anesthetics?

stage III

drug of choice for inducing anesthesia or for short procedures

Propofol (Diprivan)

PK generel anesthesia

-Distribution: throughout body; can be stored in adipose/slowly washed out!

-Elimination: lungs! So take deep breaths

*older individuals need less anesthetic

can PTs administer anesthetics?

-PTs can administer local anesthetic by phonophoresis or iontophoresis if Rx by provider

-Transdermal admin:

• Iontophoresis (electrical current)

• Phonophoresis (ultrasound)

• Patch: lidocaine -> soft tissue pain and inflammation

-peripheral nerve block

-sympathetic block

-IV regional anesthesia

-Differential nerve block

-Peripheral nerve block: effects pt ability to feel and move -> PT need to be cautious and provide support to limb with this block

-Sympathetic block: for Complex regional pain syndrome (CRPS)

-IV Regional Anesthesia: when you treat, assess damage from tourniquet

-Differential nerve block: Type C fibers; sensory modalities can be blocked without losing function (ex=epidural during labor)

anesthesia: rehab considerations

-appropriate admin of phono or iontophoresis; be alert for transdermal patches

-caution with continuous nerve blocks: loss of motor control

-local anesthesia for CRPS: schedule therapy right after to help reestablish normal SNS function and blood flow

-post epidural or spinal injections: test strength and sensation before mobilize or exercise