Medications Affecting CNS Flashcards

1
Q

Medications affecting CNS Categories

A
  1. CNS stimulants
  2. Anticonvulsants
  3. Muscle Relaxants
  4. Neuromuscular Blockers
  5. Meds for specific neurological diseases
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2
Q

CNS Stimulants

A
  1. Amphetamines
  2. Xanthines
  3. 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

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3
Q

Amphetamines

A

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)

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4
Q

Non-Stimulant For ADHD

A

-Atomoxetine (Strattera)

-inhibits reuptake of NE

Watch for Suicidal Tendencies

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5
Q

What is Clonidine used for?

A

To help patients sleep better who are taking stimulants for ADHD

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6
Q

Xanthines

A

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

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7
Q

Narcolepsy

A

-treat with stimulant type drugs that release of monoamines (specifically catecholamines NE and dopamine)

-“dafinil” family (less addictive)
1. modafinil
2. armodafinil

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8
Q

Anorexiants

A

-Using side effects of stimulants as therapeutic outcome

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9
Q

Anticonvulsants (AED’s/Antiseizure)

A

3 General Mechanisms

  1. Alter Na influx- stabilizes neuronal membrane and control of diring and seizure activity.
  2. Alter Ca influx- through special calcium channels in hypothalamus
  3. Enhance activity of GABA- can bine directly to GABA receptors, can promote GABA release, or can inhibit enzymes that normally metabolize GABA
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10
Q

Barbituate used as Anticonvulsant

A

Phenobarbital

  • old treatment and very inexpensive
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11
Q

Phenytoin (MUST KNOW)

A

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)

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12
Q

Nursing Considerations for Phenytoin

A
  • 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.
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13
Q

Therapeutic level and Toixity of Phenytoin

A

10-20mcg/mL

Toxicity: nystagmus (uncontrolled eye movement), ataxia (loss of coordination), dysarthria (difficulty speaking), ENCEPHALOPATHY (decrease in blood flow or O2 to brain)

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14
Q

What is Fosphenytoin?

A

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

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15
Q

Carbamazepine

A

-2nd most prescribed antiepiletic medication (PO use)

-ADR- hepatoxic, agranulocytosis (lack of neutrophils), and Stevens-Johnson System

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16
Q

Other Micellaneous Antiseizure Meds

A
  1. Valproic Acid- common and also used or bipolar disorder
  2. Lamotrigine (SJS warning)
  3. Levetiracetam
  4. Toprimate
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17
Q

Stevens-Johnson Syndrome (SJS)
MUST KNOW

A

RARE, serious disorder of the skin and mucous membranes. Includes: flu-like symptoms, Painful rash that spreads and blisters

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18
Q

Benzos used as Antiseizure medications

A
  • 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
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19
Q

Pregnancy and Seizures

A
  • can use magnesium sulfate

-Urine output must be greater than 30ml/hr

20
Q

Nursing Considerations for Seizures

A
  1. Assess for etiology of seizures
  2. Review labs before edministering meds (liver function and WBC)
  3. Monitor urine output (greater than 30ml/hr)
  4. If barbituate (assess resp.)
  5. Never put something in a seizing person’s mouth
  6. Institute seizure precautions
  7. Taper off meds
21
Q

Neuromuscular Blocking Agents (aka Paralytics)

A

2 different types

  1. Depolarizing- Limits acetylcholine effect at synaptic endplates and depolarizes muscle causing relaxation and paralysis
  2. 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.

22
Q

Depolarizing Neuromuscular Blocker
Only 1 Medication

A

Succinylcholine

-Used for rapid intubation

CAN CAUSE MILGNANT HYPERTHERMIA

23
Q

Nondepolarizing Neuromuscular Blockers
“curonium family”

A

MOA- Compete with ACh at nicotinic receptors, therefore prohibiting muscular contraction

-pancuronium
-vecuronium
-rocuronium

24
Q

What is the antidote for nondepolarizing neuromuscular blockers (“curoniums”)?

A

“stigmine family”

NEOSTIGMINE

25
Q

What is Malignant Hyperthermia?
MUST KNOW

A

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

26
Q

What is the antidote for malignant hyperthermia?

A

DANTROLENE

27
Q

Muscle Relaxants

A

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

28
Q

Muscle Relaxant Medications

A
  1. cyclobenzaprine
  2. methocarbamol
  3. baclofen (chronic spastic conditions)
  4. Dantrolene (directly on muscle-helps with spasticity aka muscle stiffness)
29
Q

Specific Neurological Disorders

A
  1. Migraines
  2. Parkinsons
  3. EPS relief- increased motor tone, changes in the amount and velocity of movement, and involuntary motor activity (Hypokinetic-parkinsons or Hyperkinetic-Huntingtons)
  4. Myasthenia Gravis (MG)
  5. Bell’s Palsy (BP)
  6. Alzheimers (AD)
30
Q

Migraine Headaches

A

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

31
Q

Acute Migraine Medications

A

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”
32
Q

Migraine Prophylaxis Medications

A
  • recommended if acute meds needed more than 2x per week
  1. Beta blockers (propranolol)
  2. Anticonvulsants: divalproex, lamotrigine- SJS caution and gabapentin (most common)
  3. CGRP MABS- (all end in “mab”- SC injection)
  4. Botulinum Toxin (Botox)- 15 or more HA per month
33
Q

Other Headaches

A

Cluster Headaches- triptans, ergots, high dose steroids, oxygen (12L/min)

Tension Headaches- NSAIDS or Asprin (APAP), Tricylic antidepressants

34
Q

Parkinson’s Disease

A

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

35
Q

Drugs Increasing Dopamine (Dopaminergic)

A

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

36
Q

Dopamine Receptor Agonists

A

direct stimulation of dopamine receptors

-ergots- bromocriptine

-non-ergots- generally preferred
1. pramipexole
2. rotigotine
3. ropinirol
4. apomorphine

37
Q

Other Parkinson’s Medications

A
  1. COMT Inhibitors- blocks COMT enzyme that metabolizes levodopa (tolcapone & entacapone)
    - Given only with levodopa
  2. MAO Inhibitors- blocks enzyme that breaks down dopamine (selegiline)
    - can be used single or with levodopa
  3. Anticholinergic Medication- block muscarinic receptors.
    -Used to counteract the muscle tremors and rigidity associated with dopaminergic substances
    -BENZTROPINE
38
Q

Myasthenia Gravis (MG)

A

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

39
Q

Medication for MG

A
  1. edrophonium- used to diagnose
  2. pyridostigmine- primary drug for treatment
  3. neostigmine
40
Q

Excessive Cholinergic Activity (SLUDGEM)

A

-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)

41
Q

What is the antidote for Cholinergic Crisis? (too much acetylcholine)

A

ATROPINE

42
Q

Dignosing MG

A

Tensilon Test (edrophonium)

-Results within 1 minute
-Muscles get stronger w/ positive diagnosis

MUST HAVE ATROPINE ON HAND IN CASE NEGATIVE TEST

43
Q

Bell’s Palsy

A

Etiology: viral sequelae with temporary paralysis of facial nerve virus

STEROIDS (PREDNISONE) IS DRUG OF CHOICE

44
Q

Alzheimers Disease (AD)

A

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

45
Q

First Line AD Medications

A

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

46
Q

Second Line Meds for AD

Supportive Medications

A

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