Medications Affecting CNS Flashcards
Medications affecting CNS Categories
- CNS stimulants
- Anticonvulsants
- Muscle Relaxants
- Neuromuscular Blockers
- Meds for specific neurological diseases
CNS Stimulants
- Amphetamines
- Xanthines
- Sympathomimetics
MOA- Increase stimulatory neurotransmitters or decrease inhibitory neurotransmitters
-Most common action is release of NE and Dopamine
Uses - Reverse anesthesia-induced CNS &respiratory depression; narcolepsy; ADHA; appetite suppression
ADR- insomnia, agitation, paranoia, confusion, weight lostt, tachycardia, HTN, MI (heart attack), stroke
Amphetamines
MOA- increase release of NE and dopamine
Uses- narcolepsy, ADHD, appetite suppression.
-dextroamphetamine (Dexedrine)
-dextroamphetamine/amphetamine (Adderall)
-methamphetamine- street “meth”
-methylphenidate (Ritalin)
-Concerta
-dexmethylphenidrate
-lisdexamfetamine (Vyvanse)
Daytrana (patch)
Non-Stimulant For ADHD
-Atomoxetine (Strattera)
-inhibits reuptake of NE
Watch for Suicidal Tendencies
What is Clonidine used for?
To help patients sleep better who are taking stimulants for ADHD
Xanthines
MOA- stimulates adenosine receptors in brain causing CNS stimulation, bronchodilation, and diuresis.
-Methylxanthine (CAFFEINE)
-High intake can cause abortion
USED IN PRETERM INFANTS TO REDUCE APNEA
Narcolepsy
-treat with stimulant type drugs that release of monoamines (specifically catecholamines NE and dopamine)
-“dafinil” family (less addictive)
1. modafinil
2. armodafinil
Anorexiants
-Using side effects of stimulants as therapeutic outcome
Anticonvulsants (AED’s/Antiseizure)
3 General Mechanisms
- Alter Na influx- stabilizes neuronal membrane and control of diring and seizure activity.
- Alter Ca influx- through special calcium channels in hypothalamus
- Enhance activity of GABA- can bine directly to GABA receptors, can promote GABA release, or can inhibit enzymes that normally metabolize GABA
Barbituate used as Anticonvulsant
Phenobarbital
- old treatment and very inexpensive
Phenytoin (MUST KNOW)
DRUG OF CHOICE FOR ANY TONIC/CLONIC TYPE SEIZURE
- Works on NA channels- only in neurons that are seizure generating
ADR- GINGIVAL HYPERPLASIA (overgrowth of gum tissue), also hepatotoxicity (ALT & AST)
Nursing Considerations for Phenytoin
- PO is safest route
- NOT for IM use
- BLACK BOX: CV collapse = IVP should be well- diluted and should not exceed 50mg/min - Incompatible with dextrose (flush before and after IVP).
- Very irritating to vein (check for viable IV site).
- PO given with meals; should wet mouth first to avoid direct contact of med and mucosa.
Therapeutic level and Toixity of Phenytoin
10-20mcg/mL
Toxicity: nystagmus (uncontrolled eye movement), ataxia (loss of coordination), dysarthria (difficulty speaking), ENCEPHALOPATHY (decrease in blood flow or O2 to brain)
What is Fosphenytoin?
PRODRUG- Once in the body it converts to phenytoin.
-this CAN be given IM or IV and is NOT irritating to the skin.
Same black box warning except 150mg/min
Carbamazepine
-2nd most prescribed antiepiletic medication (PO use)
-ADR- hepatoxic, agranulocytosis (lack of neutrophils), and Stevens-Johnson System
Other Micellaneous Antiseizure Meds
- Valproic Acid- common and also used or bipolar disorder
- Lamotrigine (SJS warning)
- Levetiracetam
- Toprimate
Stevens-Johnson Syndrome (SJS)
MUST KNOW
RARE, serious disorder of the skin and mucous membranes. Includes: flu-like symptoms, Painful rash that spreads and blisters
Benzos used as Antiseizure medications
- used for acute seizures (alcohol withdrawal) or status epilepticus
- quickly terminate seizures
- DIAZEPAM AKA VALIUM (LIKE AN EPI-PEN USED FOR EMERGENCY PURPOSES)
- IV RATE: Do not administer faster than 2 mg/min OR 0.05 mg/KG
-DO NOT USE FLUMENIZAL - will reverse anti-seizure effects
Pregnancy and Seizures
- can use magnesium sulfate
-Urine output must be greater than 30ml/hr
Nursing Considerations for Seizures
- Assess for etiology of seizures
- Review labs before edministering meds (liver function and WBC)
- Monitor urine output (greater than 30ml/hr)
- If barbituate (assess resp.)
- Never put something in a seizing person’s mouth
- Institute seizure precautions
- Taper off meds
Neuromuscular Blocking Agents (aka Paralytics)
2 different types
- Depolarizing- Limits acetylcholine effect at synaptic endplates and depolarizes muscle causing relaxation and paralysis
- Nondepolarizing- compete with acetylcholine at neuromuscular junction, thus resulting in inability of muscle to reach action potential for contraction
IMPORTANT- includes respiratory muscles; so need artificial ventilation.
IMPORTANT- Drugs do not cause sedation or altered LOC and do not diminish perception of pain.
Depolarizing Neuromuscular Blocker
Only 1 Medication
Succinylcholine
-Used for rapid intubation
CAN CAUSE MILGNANT HYPERTHERMIA
Nondepolarizing Neuromuscular Blockers
“curonium family”
MOA- Compete with ACh at nicotinic receptors, therefore prohibiting muscular contraction
-pancuronium
-vecuronium
-rocuronium
What is the antidote for nondepolarizing neuromuscular blockers (“curoniums”)?
“stigmine family”
NEOSTIGMINE
What is Malignant Hyperthermia?
MUST KNOW
UNCOMMON, BUT POTENTIALLY FATAL ADVERSE DRUG REACTION WHEN DEPOLARIZING NEUROMUSCULAR BLOCKING AGENTS (SUCCINYLCHOLINE) AND GENERAL ANESTHETICS (“ANE” FAMILY) ARE COMBINED
-Signs & Symptoms: RAPID rise in body temp (severe elevation), tachycardia, tachypnea, muscle rigidity
-BELIEVED TO BE GENETICALLY LINKED
What is the antidote for malignant hyperthermia?
DANTROLENE
Muscle Relaxants
MOA- unknown exactly, but overall sedative effect
-Treats muscle spasms from injury but not neurological diseases
-ADR- CNS DEPRESSION, drowsiness, dizziness, hepatotoxic
WARNING: AVOID ALCOHOL, BENZOS, AND SEDATIVES DUE TO CNS DEPRESSION
Muscle Relaxant Medications
- cyclobenzaprine
- methocarbamol
- baclofen (chronic spastic conditions)
- Dantrolene (directly on muscle-helps with spasticity aka muscle stiffness)
Specific Neurological Disorders
- Migraines
- Parkinsons
- EPS relief- increased motor tone, changes in the amount and velocity of movement, and involuntary motor activity (Hypokinetic-parkinsons or Hyperkinetic-Huntingtons)
- Myasthenia Gravis (MG)
- Bell’s Palsy (BP)
- Alzheimers (AD)
Migraine Headaches
Neurovascular origin- vasodilation and inflammation of cerebral vessels.
-imbalance of calcitonin gene-related peptide (CGRP), which promotes inflammation & headache and serotonin, which suppresses HA.
Symptoms: unilateral pain (one side), N/V, sensitivity to light
-Meds for acute HA and prophylatic
Acute Migraine Medications
The “triptans” are the drug of choice
-sumatriptan (Common)-PO, SC, or nasal spray
zolmitriptan
eletriptan
naratriptan
rizatriptan
SHOULD NOT BE USED W/ OTHER VASOCONSTRICTIVES (NICOTINE)
- “Triptans” have 2 MOA’s
1. Selective affinity for specific serotonin receptors in cerebral vessels →vasoconstriction
2. Also suppresses CGRP (calcitonin gene-related
peptide) → decrease in vascular inflammation- Can also use NSAIDS, caffeine, and “ergots”
Migraine Prophylaxis Medications
- recommended if acute meds needed more than 2x per week
- Beta blockers (propranolol)
- Anticonvulsants: divalproex, lamotrigine- SJS caution and gabapentin (most common)
- CGRP MABS- (all end in “mab”- SC injection)
- Botulinum Toxin (Botox)- 15 or more HA per month
Other Headaches
Cluster Headaches- triptans, ergots, high dose steroids, oxygen (12L/min)
Tension Headaches- NSAIDS or Asprin (APAP), Tricylic antidepressants
Parkinson’s Disease
Etiology: CNS dopamine neuron degeneration in midbrain area called substantia nigra. Creates imbalance between dopamine (inhibitory) and acetylcholine (excitatory) receptors
Decrease in dopamine and increase in acetylcholine
-So treatment is INCREASING dopamine and DECREASING acetylcholine
Drugs Increasing Dopamine (Dopaminergic)
DRUG OF CHOICE FOR PARKINSON’S- LEVODOPA/CARBIDOPA
-Dopamine aka Levodopa can not pass blood brain barrier in sufficient amounts
-Carbidopa decreases breakdown of levodopa, allowing for more lecodopa to cross into the brain and increase dopamine.
B6 VITAMIN INCREASES BREAKDOWN OF LEVODOPA
Dopamine Receptor Agonists
direct stimulation of dopamine receptors
-ergots- bromocriptine
-non-ergots- generally preferred
1. pramipexole
2. rotigotine
3. ropinirol
4. apomorphine
Other Parkinson’s Medications
- COMT Inhibitors- blocks COMT enzyme that metabolizes levodopa (tolcapone & entacapone)
- Given only with levodopa - MAO Inhibitors- blocks enzyme that breaks down dopamine (selegiline)
- can be used single or with levodopa -
Anticholinergic Medication- block muscarinic receptors.
-Used to counteract the muscle tremors and rigidity associated with dopaminergic substances
-BENZTROPINE
Myasthenia Gravis (MG)
Etiology: Disease of reduced receptors for acetylcholine resulting in muscle weakness which worsens with activity. Usually function well in early morning but progressively worsens into evening.
Treatment: cholinesterase inhibitors which result in decreased breakdown of acetylcholine, therefore more acetylcholine and enhanced cholinergic activity
Medication for MG
- edrophonium- used to diagnose
- pyridostigmine- primary drug for treatment
- neostigmine
Excessive Cholinergic Activity (SLUDGEM)
-If too much cholinesterase inhibitors, then SLUDGEM plus muscle cramps/weakness occur
Salivation (drooling)
Lacrimation (tearing)
Urinary frequency and incontinence
Defecation/Diarrhea; Diaphoresis (remember sweat glands are cholinergic)
Gastrointestinal cramps & abdominal pain
Emesis (throwing up)
Miosis (constriction of pupil)
What is the antidote for Cholinergic Crisis? (too much acetylcholine)
ATROPINE
Dignosing MG
Tensilon Test (edrophonium)
-Results within 1 minute
-Muscles get stronger w/ positive diagnosis
MUST HAVE ATROPINE ON HAND IN CASE NEGATIVE TEST
Bell’s Palsy
Etiology: viral sequelae with temporary paralysis of facial nerve virus
STEROIDS (PREDNISONE) IS DRUG OF CHOICE
Alzheimers Disease (AD)
Etiology: : Not exactly sure why, but evidence of tangled neurons in brain “Beta amyloid protein plaques” with subsequent decreased levels of the acetylcholine (ACh) in pts with Alzheimer’s.
-Results in extreme dementia.
-NO CURE
First Line AD Medications
Cholinesterase inhibitors → blocks acetylcholinesterase, the enzyme which normally breakdowns Ach = ↑ Ach
-rivatigmine
-donepezil
-galantamine
(NMDA) N-methyl-D-aspartate receptor antagonist → blocks function of these receptors in breaking down ACh → more ACh
-memantine
Second Line Meds for AD
Supportive Medications
Meds to manage hallucinations/agitation- -Antipsychotics- olanzapine, risperidone, haloperidol
Meds to manage depression
-SSRI antidepressants- fluoxetine, sertraline, citalopram
-Avoid TCA’s because of anticholinergic effects
Meds to manage sleep
-AVOID Benzos and non-benzos (zolpidem-Ambien)
-ONLY antihistamines (diphenhydramine & hydroxyzine) OR Melatonin
