Summary Quiz 2: Key Points

spasm vs spascity

-Spasm=increased involuntary tension after injury/inflammation

-Spascity= exaggerated muscle stretch reflex caused by CNS injury

Antispasmodics: generel + list meds

-NOT 1st line therapy; adjunct to rest and PT for short-term relief

-CNS depressants, cause sedative effect

-Education: Caution driving, operating machinery, fall risk; DON’T consume with alcohol (both depressants)

Meds

-Cyclobenzaprine (Flexeril)

-Diazepam (Valium)

Cyclobenzaprine (Flexeril)

spasms

-common; long half life

-AE: CNS depression=drowsiness, dizziness, lightheadedness

Diazepam (Valium)

for spasms AND spasticity

-long half life

-AE: Sedative effects, decreased mental alertness

-Fall risk, impaired driving, tolerance and dependence if prolonged use

• sudden withdrawal=seizures, anxiety, tachycardia, death

• OD=hallucinations, seizures, cardiac arrest

*increases inhibitory effect GABA; controlled substance 4 so careful of addiction

antiaspatic med list

-Baclofen (1st line treatment)

-Diazepam (Valium)

-Gapapentin

-Botox Type A

Baclofen

1st line treatment for spasicity; acts w/ spinal cord to suppress hyperactive reflexes

-CP, MS, CVA, spinal cord lesions

-Oral or pump

-AE: Drowsiness, dizziness, weakness, fatigue

• Fine line between decrease spasticity and weakness; coordinate with provider regarding balance

“other” antispasm drugs

-Gapapentin: “off label” originally for seizures

-Botox Type A: variety uses; admin via direct injection; work w/ PT same time injection to maintain long-term stretch

• Only limited amount can be administered; rare severe reactions if drug gets to systemic circulation; watch for difficulty breathing

PT Implications for spasms and spasticity

-Spasms: Drugs are complimentary to PT (drug are contraindicated for long-term use)

• manual techniques, thermal interventions, electrotherapeutic intervention

-Spasticity: Partner w/ provider regarding if drug is controlling spasms w/o causing excessive weakness

-Pt should know side effects, educate them; have them write down meds taken due to cognition

APTA spasms and spasticity

-Baclofen, Flexeril, Metazolone

-AE: hypotension, bradycardia, CNS depression

-Clinical considerations: toxicity and dysrhythmias, orthostatic hypotension, fall risk, neuromuscular impairments, cognition

NSAID: common names + therapeutic actions

-Asprin, Advil, Mortin, Aleve

-Therapeutic actions(4 A’s): antipyretic, analgesic (mild-moderate pain), anti-inflammatory, antiplatelet

• Treats: arthritis, tendonitis, fever, decreased blood clotting (low doses)

normal MOA after injury

-injury -> arachidonic acid -> cox 1 and 2 -> prostaglandins, thromboxane, prostacyclin

MOA NSAIDS

-MOA: Inhibits Cox 1 and Cox 2

• Cox1=housekeeping prostaglandins

• Cox2=select prostaglandins, turns on in response to inflammation, increases blood flow with immune cells

-Good efficacy: tend to accumulate at site of inflammation

NSAIDS: Asprin

inhibits Cox 1 and 2 but more selective for Cox1

-SE=dyspepsia/indigestion, abdominal pain, nausea/vomiting,  tinnitus, dizziness

• Blood in stool, pale

-AE=bleeding, GI ulcer, decrease kidney flood flow=kidney failure

-NEVER give to children or young adults w/ virus induced fever -> Reye’s syndrome; + Don’t give to asthmatics

-81 mg aspirin: cardioprotective effects; to be taken 2 hours before nonselective NSAID

NSAIDS: Ibuprofen

(Motrin, Advil): max 3200mg/day, 4-8 hours, 30-60 min; not big anticoagulant

-SE=dyspepsia, nausea, abdominal pain, constipation, fluid retention

-Take w/ food to prevent stomach upset

-AE= GI bleeding (less than aspirin)

-Pregnancy caution

NSAID: Naproxen

(Aleve)

freq=12 hours; rest same as Ibuprofen but….

• Half-life 14 hours, compared Ibuprofen=2-4 hours

  • Longer half life=less frequent dose

• New combination w/ acetaminophen to target pain and inflammation

NSAID: Ketoralac (Toradol)

analgesic for moderate-severe pain (often used in ED or acute care)

-SE, AE, Pregnancy: same as aspirin

NSAID: Celecoxib

only one on market; select prostaglandins bc only inhibits Cox 2

-Increases blood clotting: increased risk MI and stroke

• Vioxx removed market

-Max 200-400 mg/day

-BLACK BOX WARNING: MI or CVA

acetaminophen (Tylenol)

-NOT an NSAID bc not ant-inflammatory (or anticoagulation)

• Analgesic (mild-moderate), anti-pyretic

-Max 4g/day, Geriatric 3g/day, 6-8 hours, 30-45 min(12+; if 6-11=75 mg/kg/day)

-SE=nausea, rash, HA

-AE=hepatotoxicity: don’t take with liver disease, when fasting, or w/ alcohol

• No GI bleed or Reyes disease like NSAIDS

-Combined w/ other active ingredients in many other meds

-Pregnancy drug of choice

summary list SE NSAID

-Cox1: stomach, platelets, kidney, brain (+)

-Cox 2: kidney, brain (+), colon-rectum (+), blood vessels, injured tissue (+)

Narcotics: drug classifcications

general understanding of schedule of drugs…

-heroin and LSD 1

-oxycodone and methadone II

-tylenol with codeine III

-tramadol IV

-cough syrup V

Narcotics overview + SE

-relieve pain by binding with brain receptors and blocking pain impulses from ascending

-moderate-severe pain, pre/postop pain relief, sedation

-not chronic due to tolerance, addiction

-Typically “mu” receptors

-SE: analgesia, miosis, euphoria, constipation, respiratory depression, emesis, bradycardia

Opioid-Induced Analgesia

-Sites of Action

• Peripheral: inhibit activation spinal cord afferents

• Spinal Cord: prevent activation of spinothalamic tract

• Brain Stem: increase activation descending (inhibitory) pathway

-Opioid receptor activation: Raised pain threshold; altered brain perception of pain

Opioid common side effects (all!)

-Respiratory Depression: all pure opioid agonist cause

• want RR 12-20

• most death from respiratory arrest

-Constipation: BM last 3 days; manage with laxative and fiber

-Orthostatic hypotension: blunting of baroreceptor reflex; manage w/ education, slow transfers, gait training maybe contraindicated

-Urinary retention: urinate even if don’t have to; increases tone bladder sphincter and detrusor muscle, suppresses awareness of bladder stimuli

-Depressed renal function

-Pruitis/itchy skin

-Opiod-induced Hyeralgesia: pain worse

-Cough depression: accumulation of secretions

-Emesis: greatest w/ initial dose

-Biliary Colic: spasms common bile duct

-Elevation ICP

-Euphoria/dysphoria

-Sedation

-Miosis: constricted pupils

Comparing Opioids + Onset of Action

-Strong agonist

• morphine (rapid)

• Fentanyl (1-2 minutes): given IV, high potency

• hydromorphone/dilaudid (10-15 min)

-mod agonist

• Oxycodone: given orally, by itself=oxycontin OR w/ acetaminophen=perocet

• hydrocodone=Norco or Vicodin (10-30 min)

• codeine (30-45 min)

-weak agonist=tramadol (60 minutes), low potency and given orally

-Antagonist= naloxone (narcan)

Hydrocodone-Acetaminophen

(Norco, Vicodin): acetaminophen 325 mg, 4-6 PRN

-SE/AE: same acetaminophen and opioid section; caution pregnancy

-Caution combining w/ other acetaminophen products

-lots administration ways

PT and Opioids

-Used in all settings

-Communicate w/ pt and interdisciplinary team

-Want to find “sweet spot”: enough to decrease pain, tolerable side effects, pain relief provided may allow rehab to progress

Consider AE…

-Moniter vitals: RR 12-20, if <12 notify provider, BP/hypotension

-Assess cognition due to sedation affect; nausea

-Administered via patch: avoid heat, pressure, or exercise to area due to increase drug absorption

-Schedule therapy at peak times: regular schedule intervals (vs PRN), therapeutic plasma dose

terms:

-tolerance

-physical dependence

-addiction

-opioid withdrawl

-Tolerance: increased dose needed to produce initial response

-Physical dependence: abrupt discontinuance cause withdrawal symptoms

-Addiction: continued use of psychoactive substance despite harm

-Opioid withdrawal: symptoms

• early (yawning, rhinorrhea, diaphoresis)

• late (anorexia, irritability, tremor)

• peak (sneezing, weakness, N/V/D, muscle pain, spasms)

Naloxone (Naltrexone)

NARCAN

-opioid receptor antagonist: reverse effects (ex: respiratory depression)

-administered via NS, IM, IV

Suzetrigine

-First-in-class nonopioids: PNS and not brain; sodium channel blocker

-mod-severe pain

-avoid grapefruit!

Marijuana Effects

-short and long-term CNS impairments (cognition, memory, alertness, balance), gateway drug, cardiovascular issues (increased HR and BP), nausea

-Education vs advise as a PT

RA: generel

-Autoimmune: cytokines and TNF (meds target TNF)

-Symmetric joint stiffness and pain; joints become swollen

-Taking meds that affects immune system

RA 3 treatment goals

• Decreased joint inflammation: 

  • relieve symptoms

  • maintain function and ROM

• Decreased systemic involvement

• Delay progression of disease

RA 3 categories of drugs

• NSAIDS: pain and inflammation

• Corticosteroid: inflammation

• DMARDs: biological and nonbiologic

NSAIDS and RA

-does NOT: prevent joint damage, slow disease progression

-help pain and inflammation (rapid and short term relief)

-Cox-2

Corticosterois and RA

-help inflammation and pain (rapid relief)

• potentially slow RA progression

-short term use; bridge gap until DMARDs are onboard

-injections or oral (prednisone)

-SE: osteoporosis, infection, adrenal suppression -> AE=hypotension (so taper dose), hyperglycemia, fluid and electrolyte disturbance, peptic ulcer disease, growth suppression, cataracts

-Not just for RA

DMARDS and RA

=Disease modifying antirheumatic drugs

-Nonbiologic small molecule: chemical, cheap, easy admin=oral

• AE (bc effect immune)=anemia, neutropenia, thrombopenia, increase risk for infection

• Methotrexate: oral or injection

  • SE=rash, upset stomach, AE=bone marrow, GI ulceration, hepatic fibrosis, pneumonitis; commonly used for cancer

    • Many consider 1st choice DMARD

    • 3-6 weeks to see effects

-Biologic antibodies: biological, expensive, difficult admin=injection=quicker, moderate to severe RA

• AE=increased risk infection, decreased WBC/RBC/lymphoma/heart failure

TNF Antagonist

-Adalimumab (Humira): an injection that neutralizes TNF

-SE=injection site reactions; AE=infection (also allergic reactions, heart failure, cancer, hematologic disorders, liver injury, CNS dysfunction)

***infection can happen bc of immune system

• BOX warning: severe infection and malignancy

OA generel

-Primary (no apparent reason) vs secondary (know factor)

-Predisoposing factors: obesity, genetic susceptibility, joint vulnerability

-Treatment focused on nonpharmacological; PT, WL, joint replacement

• drugs for symptoms not disease

OA APTA support

-NO support: Glucosamine or chondroitin; Hyaluronic acid

-Strong Support:

• selective topical NSAID > oral (COX-2 inhibitors)

• non-selective NSAIDS (though Cox-2 inhibitors lower % GI adverse events)

-Inconclusive evidence: injections; acetaminophen, opioids, pain patches