Saturday, October 27, 2007

Neuro 1, Class and book notes

It's the weekend before the exam so I'm of course...finally completing my notes from the last 4 weeks. Lame!

Oct. 15: NEUROLOGICAL AGENTS; PART 2

Categories of pain:

  1. Acute: mild, moderate, or severe, lasts the length of the tissue injury.

· Mild: use nonnarcs

· Mod: use narcs and non narcs [like acetaminophen w/ codeine]

· Severe: use narcs

  1. Cancer: r/t pressure or blockage of tissues. Use NSAIDs and Narcs
  2. Chronic: persistent pain. Use nonnarcs, unless risk is fully assessed for using narcs
  3. Somatic: from muscles, bones, joints. NSAIDS are better.
  4. Superficial: from mucous membranes or integumentary damage

· Mild: use nonnarcs

· Mod: use narcs and non narcs [like acetaminophen w/ codeine]

· Severe: use narcs

  1. Vascular pain: from vascular or perivascular conditions: nonnarcs
  2. Visceral pain: body-organ related pain: nonnarcs

Post op pts: narcs and maybe NSAIDs to prevent prostaglandins

Cancer pts: narcs, and as much as they need. They do develop a tolerance. Also anxiety comes along with pain mgmt, because more pain means more metastasis

BKA amputation pt: [below knee] from diabetes usually, trauma secondly.

Phantom limb pain: nerves are still firing; so you’d give them TCA’s, antidepressant drugs, gabapentin, which is funny. Neurontin is coming up in this way…if your client is on antidepressants w/o hx, pain mgmt is probably why.

Anyone suddenly stopping seizure meds is at risk for status epilepticus

Chronic pain is usually also nerve pain: so you’re using those TCA’s, Gabapentin, etc.

Nociceptors in viscera respond more to stretching, pressure, inflammation

Tissue damage causes release of prostaglandins, bradykinin, serotonin—nociceptors respond to these and send pain signals to the brain.

Pain and vital signs: HR increases, BP decreases

Nondrug: relaxation, visualization, comfortable positioning, time manage so that you’re doing everything at once and then leave the pt alone. Shut up at the nursing station, quiet the beeping equipment.

Pain: has to be assessed. CNA’s can gather data about pain, although they can’t assess pain.

I. PAIN MANAGEMENT

A. Nonnonarcotic Analgesics: NSAIDs: non-steroidal antiinflamatory drugs are things like OTC pain killers: Ibuprofen, naproxen, etc. Good for dull throbbing pain like inflam, headaches, cramps. Act on PNS at pain receptor sites.

Not an NSAID or Narc: Acetaminophen (Tylenol); use, action; adverse effects:

Analgesic

Contra: severe hepatic or renal disease, ETOHism

Decrease pain and fevers

Inhibits prostaglandin synthesis, inhibits hypothalamic heat-regulator center [thermostat]

Adverse: hypoglycemia, oliguria, urticaria, hemorrhage, hemolytic anemia, thrombocytopenia

Liver toxic. Don’t try to kill yourself with Tylenol, you’ll just die slowly of liver toxicity. GI upset w/ all NSAIDS. Take them with some food in the stomach.

If your pt has pain meds PRN Q3 hrs, you should be assessing pain Q3hrs.

All these narcotics are lipophilic and readily cross the BBB.

PCA: best thing ever. Pts get instant relief. These pts need to be alert, educated about this medication system. Often there’s also a basal rate of small continuous dosing. These clients are still at risk for Resp and CNS depression, so these clients still need a lot of assessing.

B. Narcotic Analgesics: AKA narcotic agonists. Act largely on CNS, not PNS. Anti tussive [anti-cough] and anti-diarrheal.

1. Prototype: morphine sulfate ; use, action; adverse effects

Isolated from opium in 1803. Opium was made prescription only in 1914.

Use: acute pain, preop

Action: Depress CNS, depression of pain impulses by binding to the opiate receptor in CNS

Adverse: resp depression, seizures, increased intracranial pressure, miosis [pinned pupils], constipation, urinary retention

Always think of giving morph; it’s the gold standard narc.

All narcotics are likely to cause respiratory depression, slow GI tract. If you’ve got a patient on narcotics, you’d better know their last BM and what the laxative is to counteract it. Nurses are stingy w/ narcotics because they’ve seen someone go into resp depression.

2. Meperidine (Demerol): caution. Shorter action than morph. No anti-tussive.

Use: Not for long term use—usually 72 hours or less. In L&D it is preferred b/c it does not slow uterine contrxns. Less constipation and urine retention.

Contraindicated: Elders, cancer pts have developed neurotoxicity. Not for hepatic dysfunction, sickle cell, CAD, seizure hx, dysrhythmias. Metabolized in liver, therefore dyshepatic pts should have smaller dose.

Adverse: Don’t take it w/ other dope: CNS, resp depression risk. Long term use risk for CNS tox and seizures. Decreased BP.

3. Hydromorphone (Dilaudid): use, action, adverse effects: 6x more potent than morph—faster onset and ride. Less GI interactions, hypnotic effects. We’re using this more and more.

Use: relief of mod to severe pain

Action: like morph, depression of pain impulses by binding to the opiate receptor in CNS

Monitor respirations

Risk: CNS depression w/ other dope, ETOH

Adverse: bradycardia, tachycardia, respiratory depression [life threatening]

C. Narcotic antagonist: naloxone (Narcan): use, action, adverse effects

Use: Antidotes for overdoses of narcotics. Reverses CNS and resp depression

Action: have higher affinity to binding sites and kick the narcotics out.

Adverse: if client is in opioid withdrawal. High doses create hepatotox.

Good: approved in neonates of junkie moms.

II. ANTICONVULSANTS

Education: don’t quit taking the drugs suddenly, call if side effects show up.

Many of these drugs are teratogenic; if you want to get pregnant you’ve got to check in with some smart MD’s.

What’s w/ seizures: generalized [clonic tonic] vs partial. Generalized= all parts of the brain. These fire too spontaneously. Partial/Focal means one hemisphere. Grand mal=big bad. Absent= down LOC, can look like spacing out. Unfortunately you can only sort of blame your parents, high fevers as a child, drug withdrawals. People with chronic seizure activity are on drugs for life. Post period [posteptal] has low LOC, may need airway mgmt, rolled onto side in case of barfing.

Epilepsy: seizure disorder, 1% of pop. Abnormal electric discharges from cerebral neurons, causing loss or altered consciousness, and sometimes convulsions.

50% of epilepsy cases are thought to be primary, or of unknown origin, and the other 50% are r/t trauma, anoxia, stroke, or infection.

Grand mal: big bad, clonic tonic type.

Clonic means dysrhthmic muscle contraction, tonic means sustained muscle contraction

Petit mal: tiny bad, ‘absence’ type. Means brief loss of consciousness.

Psychomotor: complex symptoms: repetitive behaviors, motor seizure, behavioral changes

Status epilepticus: emergency seizures in rapid succession: a continuous seizure that will not stop without intervention. Pregnancy eclampsia, meningitis, or toxic stuff. Or withdrawal from anti-convulsants.

A. Hydantoins; Prototype: phenytoin (dilantin); Anti convulsant

Use: grand mal, partial complex seizures

Action: reducing motor cortex activity by altering transport of ions.

Adverse: least toxic effects. Aplastic anemia, Thrombocytopenia, ventricular fib. Bleeding disorders from not enough platelets, H&H. Teratogenic.

B. Barbituates: now used more for ‘status epilepticus:’ when there’s a long seizure that’s emergent.

C. Benzodiazepines now used more for ‘status epilepticus:’ when there’s a long seizure that’s emergent.

D. Valproate: Valproic acid: Rxed for various types of seizures. Hepatotoxic.

Prototype: Gabapentin/Neurontin

Use: is a medication originally developed for the treatment of epilepsy. Presently, gabapentin is widely used to relieve pain, especially neuropathic pain.

Action: was made to mimic GABA, but it doesn’t work that way. Its exact mechanism of action is unknown, but its therapeutic action on neuropathic pain is thought to involve voltage-gated N-type calcium ion channels. Book says “promotes GABA release”

Adverse: nothing too exciting. Best eaten with food.

E. Case Scenarios

III. NEUROLOGICAL DISORDERS

A. Parkinsonism: serious disease. Involuntary tremors, movements, cerebral function is the same; don’t assume they have altered cognitive function. Imbalance of acetylcholine [short term memory, muscles, PNS] and dopamine. Acetylcholine is excitatory or activating NT, dopamine is an inhibitory NT. Lack of dopamine at pre-synaptic muscle receptors. Advanced stages can create confusion. Degradation of the dopamine secreting neurons in the substantia nigra

Dopaminergic Drugs:

Prototype; carbidopa-levodopa (Sinemet): helps balance out lack of dopamine

Use: anti-parkinson; tremors and rigidity

Action: levodopa turns to Dopamine in the brain. Carbidopa inhibits levodopa from turning to dopamine in the rest of the body.

Adverse: palpitations, psychosis, hallucinations, depressions

Life threatening: hemolytic anemia, agranulocytosis, dysrhthmias

B. Alzheimer’s Disease: really prevalent pathophysiological syndrome. Stanford just came up with a pre-Alzheimer’s blood test; which can be helpful in terms of planning and prophylactic medication.

1. Pathology: Lack of acetylcholine. Caused by malformed neural microtubules, crumbling cells. Genetic predisposition. It’s just one type of dementia; forgetfulness; these guys can tell you all about WW2 but not remember breakfast. Incontinence and fall risks also increase b/c motor skills decrease. Wandering happens too. Exercise and mental activity help prevent Alzheimer’s by taking blood to brain.

Acetylcholinesterase inhibitors: block the enzyme from breaking down acetylcholine [which you need]

2. prototype: tacrine Cognex.

Use: alzheimers, memory loss, Myasthenia Gravis

Action: elevates Ach by blocking the Ach breaker-downer enzyme

Adverse: depression, hepatotox

IV. NEUROMUSCULAR DISORDERS

A. Myasthenia Gravis: autoimmune, effects young women, lack of acetylcholine, lack of nerve impulses are myoneural junction; the nerves want to talk but they lost their cell phone [Ach]. Use Acetylcholinesterase inhibitors for this too.

B. Multiple Sclerosis: demyelination of neurons in CNS and PNS, also effects young white girls. Use muscle relaxants for this.

V. PSYCHIATRIC AGENTS

Lots and lots of drugs.

Depression is the most common chronic illness second to HTN [most common psych disorder: anxiety.]

Schizophrenia: disorganized thoughts and behaviors.

Just because you don’t want to be a psych nurse doesn’t mean psych patients won’t end up on your floor sick or getting surgery.

A. Antispychotics: there’s a laundry list of these drugs

1. Phenothiazines: fluphenazine (Prolixin): use, action, adverse effects increase the longer people are on the drugs, EPS symptoms, dyskinesia

Use: psychosis, schizophrenia

Action: blocks dopamine receptors in brain

Adverse: Agranulocytosis, EPS [parkinson’s-esque], tachycardia

NCLEX and quiz question: Phenothizazines have anticholinergic [pro SNS] effects:

Phenothiazines have combined anticholinergic and central thermoregulatory effects.

phenothiazines have anticholinergic effects, they should not be used in combination with other drugs that may have similar effects.

phenothiazines have prominent anticholinergic properties that may cause delirium.

Anticholinergic drugs or drugs with anticholinergic effects are frequently associated with hyperpyrexia and heat illness. These drugs inhibit sweating, thereby reducing heat elimination.[3] Other anticholinergic effects include tachycardia, dry flushed skin, dilated pupils, decreased gastrointestinal motility, and urinary retention. In anticholinergic overdose, mental status changes with delirium may be present. Seizures, myoclonus, and dysrhythmias can also occur.

2. Nonphenothiazines: haloperidol (Haldol): use, action, adverse effects

Use: neuroleptic that stabilizes thinking processes for confusion and psychosis, Tourette’s

Action: Book says it changes how dopamine acts on CNS. Margi says: blocks dopamine receptors in CNS. Resp depression.

Adverse: laryngospasm, resp depression, dysrhthymias, neuromalignant syndrome

B. Anxiolytics: anti-anxiety, some people have such acute anxiety they can’t leave the house.

1. Benzodiazepines: lorazepam (Ativan): Benzos are great: are used for panic attacks, severe or prolonged anxiety, depression, insomnia, seizures, ETOH withdrawal, skeletal muscle spasm, pre-op meds. Fewer side effects than barbs. Risky long term

use: anti-anxiety, anti-emetic, preop, status epilepticus

action: potentiate GABA effects by binding to specific GABA/benzo receptors; The main pharmacological effects of lorazepam are the enhancement of GABA at the GABAA receptor. I think the book might have eaten some ativan when they wrote out the drug action—it doesn’t sound right.

Adverse effects : fewer than other benzos. These cause amnesia when the drug is on board. Tolerance can be developed. CNS depression, resp depression, hypotension esp when hypovolemic.

2. Buspirone hydrochloride (BuSpar): use, action, adverse effects: better long term than ativan. effective after 1-2 weeks, fewer side effects.

Use: generalized anxiety

Action: It is thought to act by interfering with the function of the neurotransmitter serotonin in the brain, particularly by serving as a 5-HT1A receptor partial agonist. Additionally, it acts as a mixed agonist/antagonist on postsynaptic dopamine receptor

Side effects; less withdrawal than benzos.

Adverse: subdermal bleeding, extrapyramidal symptoms, hallucinations, psychosis, ataxia, epileptic seizures, syncope, tunnel vision, urine retention, alopecia, pruritus, hot flashes.

VI. ANTIDEPRESSANTS

All can cause suicidal tendencies

A. Depression: #2 most common chronic condition.

Reactive depression: after grieving, after major events. Usually need pharma until the NTs recover on their own.

If you have a pt w/ Hx of depression: what are their meds, do they treat with therapies, assess if they are feeling depressed, the chaplains are great non-denominational listeners

People don’t rehab or get well when they’re depressed.

Major depression: lack of motivation, interest

Bipolar: Manic and then Depressed

B. Drugs

1. TCAs: amitriptyline (Elavil):

use: depression, bipolar, migraines,

action: serotonin and norepinephrine increased in nerve cells by blocking nerve fibers

adverse effects: seizures, agranulocytosis, thrombocytopenia

2. SSRIs: fluoxetine (Prozac): serotonin synaptic reuptake inhibitors

use: depression, bipolar, migraines

action: serotonin is increased in neurons by blocking reuptake: These don’t let them go back to the house on the pre-synaptic neuron, so it’s in the synapse longer. People w/ chronic depression often have serotonin-not-enough-syndrome

adverse effects :. Seizures

3. MAOIs: these are bad bad. High risk of interactions. Amino-amine-oxidase inhibitors, that break down epi and nor epi. HTN crisis. These interact w/ everything including cheese and wine. Old anti-depressants.

C. Mood Stabilizer: Lithium for bipolar disorder; use, action, adverse effects

Use; manic episodes, bipolar.

Action: ion transport in muscle and nerve cells, increased receptor sensitivity to serotonin

Adverse: dysrhthymias, circulatory collapse

At the completion of this class, the student will be able to:

1. Distinguish between nonnarcotic and narcotic analgesia and state indications for both;

2. discuss actions, uses, and adverse effects of specific opioids;

3. distinguish between the types of seizures;

4. describe use, action, and adverse effects of anticonvulsant drugs;

5. describe the actions and adverse effects of antiparkinson and Alzheimer’s disease drugs;

6. explain treatment strategies for multiple sclerosis and myasthenia gravis;

7. describe use, action, and adverse effects of antipsychotics and anxiolytics;

8. discuss use, action, and adverse effects of antidepressants;

9. discuss key patient teaching with safe use of these drugs.

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