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47 Cards in this Set

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Define analgesia
a medication that relieves pain without causing the loss of consciousness. the most common are opiods and NSAIDs
Define anesthesia.
Loss of the ability to feel pain, resulting from the administration of an anesthetic drug or other medication intervention
Describe the basic differences between general and local anesthesia.
General anesthesia- Drugs tha induce a state in which the CNS is altered to produce varying degrees of:
Pain relief
Depression of consciousness
Skeletal muscle relaxation
Reflex reduction

Local Anesthetics- Used to render a specific portion of the body insensitive to pain
Interfere with nerve impulse transmission to specific areas of the body
Do not cause loss of consciousness
List the most commonly used general and local anesthetics and their associated risks.
General anesthetics-
enflurane (Ethrane), halothane (Fluthane), isoflurane (Forane), methoxyflurane (Pentharane), nitrous oxide "laughing gas", propofol (Diprivan), sevoflurane (Ultane).

Local anesthetics-Lidocaine (Xylocaine)
Compare the mechanisms of action, indications, adverse effects, routes of administration, cautions, contraindications, and drug interactions of local anesthesia.
action-work by rendering a specific portion of the body insensitive to pain by interfering with nerve transmission in that area.

indications-surgical, dental, or diagnostic procedurs, various types of chronic pain.

adverse effects-limited, undesirable effects, "spinal headache"

contraindications-known drug allergy
drug interactions-few significant, with certain drugs can lead to dysrhythmias

routes of administration-esters and amides, classified as topical or parenteral (injectable)
Describe the impact of CNS depressants on all body systems.
Barbiturates: brainstem (reticular formation); inhibiting GABA, nerve impulses traveling in the cerebral cortex are also inhibited
Cardiovascular-vasodialation and hypotension
GI-nausea, vomiting, diarrhea, constipation
Hemat-Agranulocytosis, thrombocytopenia, magaloblastic anemia
Nervous-drowsiness, lethargy, vertigo, headache, mental depression etc
Respiratory-respiratory depression, apnea, laryngospasm, brochospasm, coughing

Benzodiazepines:affect hypothalemic, thalamic, and limbic systems of the brain, do not suppress REM sleep as much as barbiturates do; do not increase metabolism of other drugs
Differentiate between the following terms: sedative-hypnotic drugs, barbiturates, benzodiazepines, muscle relaxants, and non-benzodiazepine drugs.
Sedative-hypnotic drugs- drugs that can act in the body either as sedatives or as hypnotics.
Barbiturates- a class of drugs tat are chemical derivatives of barbituric acid. they can induce sedation and sleep.

Benxodiazepines- a chemical category of drugs most frequently prescribed as sedative-hypnotic and anxiolytic drugs.

Muscle relaxants-a group of compounds tha act predominantly within the CNS to relieve pain associated with skeletal muscle spasms.

Non-benzodiazepine drugs-pharmacologic properties of these drugs are similar to those of benzodiazepines in that they have sedative, anxiolytic, muscle relaxant, and anticonvulsive effects, they are indicated fro the short-terms treatment of insomnia, are only available orally, and are designated as Schedule 4 controlled substances.
Identify the specific drugs within each category of CNS depressants.
Barbiturates-butabarbital (butisol), pentobarbital (Nembutol), phenobarbital (luminal), secobarbital (Seconal)

Benzodiazepines-estazolam (ProSom), flurazepam (dalmane), quazepam (Doral), temazepam (Restoril), triazolam (Halcion)

Muscle relaxants-baclofen (Lioresal), cyclobenzaprine (Flexeril), dentrolene (dantrium)

Non-benzodiazepines-zalepion (Sonata), zolpidem (Ambien), and eszoplizone (Lunesta)

Non-barbiturates-chloral hydrate (Noctec)
Discuss nonpharmacologic approaches to the treatment of sleep disorders.
Establish as set sleep pattern with a time to go to bed and a regular time to get up. Sleep only as much as you need to feel refreshed and renewed.
Keep bed room temp moderate.
Avoid caffeine-containing beverages and food within 6 hrs of bedtime.
Decrease exposure to loud noises.
Avoid daytime napping.
Avoid exercis late in the evening.
Avoid alcohol in the evening (fragmented sleep).
Avoid tobacco at bedtime.
Try to relax before bedtime with soft music, yoga, etc.
Drink a warm decaffeinated beverage, warm milk 30 min to 1 hr before bed.
If you are still awake 20 min after going to bed get up and engage in a relaxing activity and go back to bed once you feel drowsy, repeat as necessary.
Discuss the rationale for use of the various classes of antiepileptic drugs (AEDs) used in the management of the various forms of epilepsy.
The cause of more than 50% of the cases of epilepsy is unknown. That type of epilepsy for which a cause cannot be identified is called primary or idiopathic epilepsy. Other types of epilepsy have a distinct cause such as trauma, infection, cerebro-vascular disorder, or other illness. These types of epilepsy are called secondary epilepsy.


The combined goal of AED therapy is to control or prevent seizures while maintaining a reasonable quality of life. Approximately 70% of patients can expect to become seizure-free with modern drug therapy, and most will only take one AED. The remaining 30% of cases are more complicated, often requiring additional medications. Many AEDs have adverse effects, and balancing seizure control with adverse effects is often a difficult task. In most cases, the therapeutic goal is not to eliminate seizure activity but rather to maximally reduce the incidence of seizures while minimizing drug-induced toxicity.
Identify the various drugs within each of the following drug classes: iminostilbenes, benzodiazepines, barbiturates, hydantoins, and miscellaneous.
Iminostilbenes: carbamazepine (Tegretol, Tegretol XD); 2nd most commonly prescribed AED in the US

Hydantoins: phenytoin (Dilantin) has been used as a first-line AED for many years. It is primarily indicated for the management of tonic-clonic and parital seizures. ***SPECAL NOTICE*** With IV phenytoin (Dilantin) use only NS with the push. Other drugs or soln can cause complications at IV site and destruction to vein. ALSO, use of this drug requires extra special oral care as is known to cause gingival hyperplasia or swollen red bleeding gums.

benzodiazapine: diazapam (Valium) is considered the drug of choice for Status epilepticus (Status epilepticus is a common seizure disorder that is a life-threatening emergency; it is characterized by generalized tonic-clonic convulsions that occur in succession. Affected patients typically do not regain consciousness between the many convulsions.)

barbituates: two of the most commonly used AEDs were the barbiturates phenobarbital (Solfoton) and primidone (Mysoline). Phenobarbital has been used since 1912, principally for controlling tonic-clonic and partial seizures. Phenobarbital is still one of the fi rst-line drugs for the management of status epilepticus and is an effective prophylactic drug for the control of febrile seizures.
Identify the mechanisms of action, indications, cautions, contraindications, dosages, routes of administration, adverse effects, toxic effects, any related serum therapeutic levels and drug interactions for the various drugs within the different classifications of AEDs.
MoA: AEDs result in stabilized and less responsive cell membranes which prevents generation and spread of excessive electrical discharge from abnormally functioning nerve cells. Neurons are stablized & hyperexcitablity is decreased.

Indications: prevention or control of seizure activity (but NOT cure); long-term maintenance for chronic, recurring seizures; acute Rx of convulsions and status epilepticus

Cautions/Contraindications: The only usual contraindication to AEDs is known drug allergy. Pregnancy is also a common contraindication. AEDs are plagued by many adverse effects, which often limit their usefulness. AA include: Apnea, hypotension, somnolence, cardiac dysrhythmias, hypotension (only few)

dosage:
Diazepam0.3-0.5 mg/kg
Phenobarbital15-20 mg/kg

routes: enteral (Clonopine) and parenteral (pheytoins) depending on drug needed
Briefly discuss the pathophysiology related to Parkinson's disease (PD).
Parkinson’s disease (PD) is a chronic, progressive, degenerative disorder affecting the dopamine-producing neurons in the brain
It is now recognized that PD results from an imbalance in two neurotransmitters—dopamine (DA) and acetylcholine (ACh)—in the basal ganglia. This imbalance is caused by failure of the nerve terminals in the substantia nigra to produce the essential neurotransmitter dopamine. This neurotransmitter acts in the basal ganglia to control movements. Destruction of the substantia nigra leads to dopamine depletion. Dopamine is an inhibitory neurotransmitter, and ACh is an excitatory neurotransmitter in this area of the brain. A correct balance between these two neu-rotransmitters is needed for the proper regulation of posture, muscle tone, and voluntary movement.
Identify the different classes of medications used as antiparkinsonian drugs, including first and second line of drugs used in therapy.
Dopamine receptor agonists: levodopa, levodopa-carbidopa,

Indirect-Acting Dopamine Receptor Agonists:
MAO-B: inhibitor selegiline
Miscellaneous: amantadine

Nonselective MAOIs such as MAO-A and MAO-B were initially used to treat however a major adverse effect is the interaction wity tyramine-containing foods (cheese, red wine, beer, and yogurt) resulting in severe hypertension

Selegiline was introduced in 1974 and in 1989 was approved by the FDA for use inconjunction with levodopa therapy.

Levodopa and Levodopa-carbidopa are considered the cornerstone of treatment in PD as Levodopa is the precursor of dopamine required by the brain for dopamine synthesis. They are known as presynaptic or replacement drugs.
Identify the various psychotherapeutic drugs: antianxiety drugs
Antianxiety Drugs: Benzodiazepines are the largest and most commonly pre-scribed anxiolytic drug class because they offer several advan-tages over the other drug classes used to treat anxiety. Commonly prescribed anxiolytic benzodiazepines are diazepam (Valium), lorazepam (Ativan), alprazolam (Xanax), clonazepam (Klono-pin), chlordiazepoxide (Librium), and midazolam (Versed).
Drug Profile: TCA's
TCAs are believed to work by correcting the imbalance in the neurotransmitter concentrations of serotonin and norepinephrine at the nerve endings in the CNS. This is accomplished by blocking the reuptake of the neurotrans-mitters and thus causing these neurotransmitters to accumulate at the nerve endings.

TCAs have several advantageous therapeutic effects, but their use is also associated with many adverse effects.

TCAs are used to treat depression. They have been available for more than 40 years. Overall, they have demonstrated a remarkable effi cacy, and their adverse-effect profi les are well established.

Contraindications for TCAs include known drug allergy, use sooner than 14 days after stopping MAOI therapy, and pregnancy. They are also not recommended in patients with any acute or chronic cardiac problems or seizure history

TCAs results in many undesirable anti-cholinergic adverse effects, the most common being sedation, impotence, and orthostatic hypotension

TCA overdoses are notoriously lethal. It is estimated that 70% to 80% of patients who die of TCA overdose do so before reaching the hospital.

Drug interaction noted in use with warfarin; may cause excessive bleeding, possibly to death. And also with use of St. John's wart- causes GI upset, allergic reactions, fatique, dizziness, and so forth
Identify the various central nervous system (CNS) stimulants and their indications, contraindications, cautions, and drug interactions.
For ADHD: amphetamine (Adderall), methylpehnidate (Concerta, Ritalin); atomoxetine (Strattera)

For Narcolepsy: modafinil (Provigil)

For Obesity: Anorexiants; sibutramine (Meridia - newest on the market); phetermine (lonamin);

For Migraine: Serotonin agonists: sumatriptan (Imitrex) used to treat but will not prevent;

CNS Stimulants can also include analeptics; doxapram (Dopram), methylxanthines such as theophylline, aminophylline are used as breathing treatments.

Caffeine: found in foods, OTC drugs, some prescript drugs
Discuss the therapeutic effects and adverse effects associated with the use of CNS stimulants.
CNS stimulants elevate mood, produce a sense of increased energy and alertness, decrease appetite, and enhance task performance impaired by fatigue or boredom.

Adverse effects include: palpitations, tachycardia, hypertension, angina, dysrythmias, nervousness, restlessness, anxiety, insomnia, nausea, vomitting, diarrhea, dry mouth, increased urinary frequency,
Briefly describe the mechanisms of action, dosage forms, routes of administration, adverse effects, toxic effects, cautions, contraindications, and drug interactions associated with the various CNS stimulants.
Amphetamines stimulate areas of the brain associated with men-tal alertness, such as the cerebral cortex and the thalamus. The pharmacologic actions of amphetamines and sympathomimetic CNS stimulants are similar to the actions of the SNS in that the CNS and respiratory system are the primary body systems af-fected. CNS effects include mood elevation or euphoria, in-creased mental alertness and capacity for work, decreased fatigue and drowsiness, and prolonged wakefulness. The respiratory ef-fects most commonly seen are relaxation of bronchial smooth muscle, increased respiration, and dilation of pulmonary arteries

The primary route of admin is PO in form of a tablet. Dosage varies depending on particular medication and treatment.
Mechanism of Action and Drug Effects: Levodopa and Levodopa-carbidopa
Traditionally, very large doses of le-vodopa had to be administered to get enough dopamine to the brain because much of the levodopa administered was broken down outside the CNS by this same enzyme. These large doses resulted in high peripheral levels of dopamine and many un-wanted adverse effects such as confusion, involuntary move-ments, gastrointestinal (GI) distress, and hypotension. Levodopa has even been known to cause dysrhythmias. These problems are avoided when levodopa is given with carbidopa, a peripheral de-carboxylase inhibitor that does not cross the blood-brain barrier. Therefore, carbidopa prevents levodopa breakdown in the pe-riphery. As a result, levodopa is allowed to reach and cross the blood-brain barrier, yet carbidopa does not cross this barrier. Once in the brain, the levodopa is then converted to dopamine, which can then exert its therapeutic antiparkinsonian effects by offsetting the dopamine ACh imbalance.
PD Drug Profile - Amantadine (Symmetrel)
Amantadine (Symmetrel) is believed to work in the CNS by eliciting the release of dopamine from nerve endings, causing higher concentrations of dopamine in the CNS. It is most effective in the earlier stages of PD when there are still significant numbers of nerves to act on and dopamine to be released. As the disease progresses, however, the population of functioning nerves diminishes, and so does amantadine’s effect. Amantadine is usually effective for only 6 to 12 months. After amantadine fails to relieve the hypokinesia and rigidity, a dopamine agonist such as bromocriptine or pergolide is usually tried next.
PD Drug Profile - Selegiline (Eldepryl)
Selegiline (Eldepryl) is an MAO-B inhibitor used as an adjunctive drug along with levodopa to decrease the
amount of levodopa needed.

The most common adverse effects associated with selegiline use are mild and consist of nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion, and dry mouth.
PD Drug Profile - Anticholergics
drugs that block the effects of ACh, are sometimes useful in treating the muscle tremors and muscle rigidity associated with PD. These two symptoms are caused by excessive cholinergic activity, which occurs due to lack of the normal dopamine balance

The rationale for the use of anticholinergics is to reduce excessive cholinergic activity in the brain. The first drugs in this category to be used were the belladonna alkaloids, atropine and scopolamine. However the anticholinergic adverse effects of dry mouth, urinary retention, and blurred vision can be excessive; therefore, new synthetic anticholinergics and antihistamines with better adverse effect profiles
Implementation of PD drugs:
Key factors/considerations
Oral doses should be given with food to help minimize GI Upset.
What is a drug holiday?
A drug holiday (usually a 10-day pe-riod) is sometimes used by physicians when drug therapy is not working. The patient is generally hospitalized so that when the drug is withdrawn and the patient is without drugs, he or she can be taken care of appropriately and have needs met. Depending on the severity of the disease process, a patient may be totally de-pendent on others for basic care and nutritional and elimination needs. A patient may even be immobilized by a contracted physi-cal state and not able to turn in bed, thus requiring a controlled environment with around-the-clock medical and nursing care. The purpose for the drug holiday is to hopefully obtain more therapeutic effectiveness once the levodopa is “re-initiated,” and the hope is also for the patient to respond to a lower dose of the drug.
Which of the following should alert the nurse to a potential caution or contraindication with use of a dopaminergic drug for treatment of mild PD?
a. Diarrhea
b. Tremors
c. Narrow angle glaucoma
d. Unstable gait
C. narrow-angle glaucoma

p. 213
A patient is taking entacapone as part of the therapy for Parkinson’s disease. Which intervention is appropriate at this time?
a. Notify the patient that this drug causes discoloration of the urine.
b. Limit the patient’s intake of tyramine-containing foods.
c. Monitor liver studies as this drug can seriously affect liver function.
d. Force fluids to prevent dehydration.
a. Notify the patient that this drug causes discoloration of the urine.

pg 214; Table 14-4
Patient teaching for antiparkinsonian drugs should include which statements?
a. The drug should be stopped when tremors and weakness are relieved.
b. If a dose is missed, take two doses to avoid significant decreases in blood levels.
c. Notify the physician if the urine turns brownish-orange in color.
d. Change positions slowly to prevent falling due to postural hypotension.
d. Change positions slowly to prevent falling due to postural hypotension.

pg 220; Pt Teaching tips
Which statement is true regarding new drug therapy for a patient who has PD and is not responding well to levodopa therapy:
a. Adding haloperidol (Haldol) will reduce adverse effects of levodopa.
b. Taking methyldopa (Aldomet) will increase available dopamine levels in the brain.
c. Taking amantadine (Symmetrel) improves the effectiveness of levodopa.
d. Adding carbidopa will prevent the peripheral destruction of levodopa and result in increased amounts in the brain
d. Adding carbidopa will prevent the peripheral destruction of le-vodopa and result in increased amounts in the brain

pg 213
Which statement should be included during patient teaching about the use of levodopa-carbidopa?
a. There are very few drug interactions with levodopa-carbidopa.
b. Therapeutic effects may take up to several weeks to a few months.
c. Notify the physician immediately if darkening of urine or sweat occurs.
d. Pyridoxine (vitamin B6) helps protect the action of levodopa-carbidopa.
b. Therapeutic effects may take up to several weeks to a few months.
Define: attention deficit disorder
Syndrome affecting children, adolescents, and adults that involves difficulty in maintaining concentration on a given task and/or hyperactive behavior. The term attention deficit disorder (ADD) has been absorbed under this broader term. (p. 253)
Define: anorexiant
Drugs used to control or suppress appetite. These also stimulate the CNS. (p. 257)
Define: hyperactivity
An abnormally high level of activity or excitement shown by a person, especially a child, that interferes with the ability to concentrate or interact with others
Define: attention deficit hyperactivity disorder (ADHD)
Syndrome affecting children, adolescents, and adults that involves difficulty in maintaining concentration on a given task and/or hyperactive behavior. The term attention deficit disorder (ADD) has been absorbed under this broader term. (p. 253)
Define: obesity
The condition of being obese; increased body weight caused by excessive accumulation of fat
Define: Migraine Headache
A common type of recurring painful headache characterized by a pulsatile or throbbing quality, incapacitat-ing pain, and photophobia. (p. 259)
Identify the various psychotherapeutic drugs: antidepressants
Most commonly used are the Selective Serotonin Reuptake inhibitors (SSRI)s and the second and third generation antidepressants. Less commonly used are what are considered to be, the first generation antidepressants.

These include the TCAs and MAOIs.

2nd gen: trazadone (Desyrel), bupropion (Wellbutrin), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft).

3rd gen: SSRI (Effexor)
Identify the various psychotherapeutic drugs: antimaniac
The original drugs currently available that can effectively alleviate the major symptoms of mania are the lithium salts. Lithium also continues to be shown effective in maintenance treatment of Bi polar disorder. It is considered the standard for other antimaniacs. It is often used in conjunction with other medications to stabilize the mood. Lithium however has narrow therapeutic index with increases potential risk for toxicity.
Identify the various psychotherapeutic drugs: antipsychotics
Constituting about two thirds of all antipsychotics, phenothiazines are the largest group of antipsychotic drugs. Like many other drugs, phenothiazines were discovered by chance, in this case during research for new antihistamines. In 1951, chlorpromazine was the first phenothiazine to be discovered in this way. Phenothiazines are associated with a high incidence of anticholinergic adverse effects because they are so closely related to antihistamines.
Drug Profile: MAOI's
Two available MAOI antidepressants, phenelzine (Nardil) and tranylcypromine (Parnate), are nonselective inhibitors of both types A and B MAO. Both types of MAO are widely distributed throughout the body, including the brain. MAO-A preferentially metabolizes serotonin, norepinephrine, and tyramine. MAO-B preferentially metabolizes dopamine. By inhibiting the MAO en-zyme system in the CNS of patients suffering from depression, amines such as dopamine, serotonin, and norepinephrine are not broken down, and, therefore, higher levels occur. This in turn al-leviates the symptoms of depression. However, higher levels of tyramine can also result in the hazardous drug-food interactions associated with MAOIs. It should be noted that MAOIs, as with other antidepressants, might take 1 to 4 weeks or more to reach their full therapeutic effects. A wide variety of drug interactions can occur with MAOIs. Sym-pathomimetic drugs can also interact with the MAOIs and to-gether cause a hypertensive crisis. MAOIs can markedly potenti-ate the effects of meperidine, and, therefore, concurrent use is contraindicated. In addition, concurrent use of MAOIs with SSRIs carries the risk for serotonin syndrome which can lead to delirium in the patient.
Drug Profile: General antipsychotics
Penothiazine is the largest group. These work as dopamine receptor blockers in the brain - areas associated with emotion, cognitive function and motor function. Too much dopamine in the brain can bring about psychosis. Indications are BPD, Schizophrenia, Autism, Tourette's. Potential Adverse affects are sedation, delirium, orthostatic hypotension, drowsiness, neuroleptic malignant syndrome (NMS), extrapyramidal symptoms (EPS), and tardive dyskinesia (TD). NMS is a potentially life-threatening adverse effect that may include high fever, unstable blood pressure (BP), and myoglobinemia. EPS involves involuntary motor symptoms similar to those associated with Parkinson’s disease. Tardive is a word that means “late-appearing.” TD involves involuntary contractions of oral and facial muscles. Also includes choreoathetosis (wavelike movements of extremities) that usually appears only after continuous long-term antipsychotic therapy.
Contrast the mechanism of action, indications, adverse effects, toxic effects, cautions, contraindications, dosage forms, routes of administration, and drug interactions of barbiturates.
action-CNS depressants that act primarily on the brain-stem in an area called the reticular formation, act by reducing the nerve impulses traveling to the area of the brain called the cerebral cortex.

indications-hypnotics, sedatives, anticonvulsants and also for anesthesia during surgical procedures.

adverse effects-drowsiness, lethargy, dizziness, hangover, and paradoxical restlessness or excitement.

toxic effects-respiratory depression leading to respiratory arrest

cautions-

contraindications-known drug allergy, pregnancy, significan respiratory difficulties, and sever liver disease.

dosage forms-sedative or hypnotics depending on the dosage

routes of administration-PO, IM, IV, rectal.
Contrast the mechanism of action, indications, adverse effects, toxic effects, cautions, contraindications, dosage forms, routes of administration, and drug interactions of benzodiazepines.
action-sedative and hypnotic action related to their ability to depress activity in the CNS, inhibit stimulation of the brain, affect the hypothalamic, thalamic, and limbic systems of the brain

indications-sedation, sleep induction, skeletal muscle relaxation, and anxiety relief, alcohol with drawal, agitation, depression, and epilepsy.

adverse effects-relatively safe, headache, drowsiness, paradoxical excitement or nervousness, dizziness, or vertigo, congnitive impairment, and lethargy.

toxic effects-somnolence, confusion, coma and diminished reflexes, rarely results in death. Flumazenil antagonizes.

cautions-can create a fall hazard in frail elderly patients

contraindications-known drug allergy, narrow-angle glaucoma, and pregnancy

dosage forms-should be limited to short-terms of 2 to 4 weeks or less, low doses in elderly pt

routes of administration-PO
Contrast the mechanism of action, indications, adverse effects, toxic effects, cautions, contraindications, dosage forms, routes of administration, and drug interactions of muscle relaxants.
action-CNS depression in the brain primarily at the level of the brainstem, thalamus, and basal ganglia, also spinal cord. effects are relaxation of striated muscle contractions, and muscle stiffness.

indications-relief of painful muscoloskeletal conditions such as muscle spasms, management of spasticity (associated w/ multiple sclerosis, cerebral palsy, etc), malignant hyperthermia crisis, relieving hiccups

adverse effects-euphoria lightheadedness, dizziness, drowsiness, fatigue, and muscle weakness.

toxic effects-no specific antidote or reversal drug, treated with conservative supportive measures.

contraindications-known drug allergy, some drugs may als include severe renal impairment.

routes of administration-PO, IV, intrathecal
Compare the mechanisms of action, indications, adverse effects, routes of administration, cautions, contraindications, and drug interactions of general anesthesia.
action-Overton-Meyer therory strates that there is a relationship between the lipid solubility of an anesthetic drug and its potency:the greater the solubility of the drug in fat, the greater the effect. nerve cell membranes have a high lipid content, as does the blood-brain barrier, lipid-soluble anesthetic drugs can therefor easily cross the blood-brain barrier and concentrate in nerve cell membranes.

indications-used to produce unconsciousness, skeletal muscular relaxation, and visceral smooth muscle relaxation for surgical procedures

adverse effects-dose dependent, vary with the individual drug, heart, peripheral circulation, liver, kidneys, and respiratory tract, Myocardial depression, hapatotoxicity

contraindications-known drug allergy, pregnancy, marrow-angle glaucoma, known susceptibility to malignant hyperthermia

drug interactions-antihypertensives, b-blockers, and tetracycline-cause additive effects. antihypertensives may lead to increased hypotensive effects, b-blockers-increased myocardial depression, tetracycline- increased renal toxicity

routes of administration-inhalation general anesthetic
Compare the mechanisms of action, indications, adverse effects, routes of administration, cautions, contraindications, and drug interactions for drugs used for moderate/conscious sedation.
action-an anesthesia that does not lead to loss of consciousness.

indications-allows pt to remain conscius, respond verbally to commands, relax, and maintain an open airway.

adverse effects-more rapid recovery time tha general anesthesia, better safety profile becaus of lower cardiopulmonary risk. Mild amnesia may occur

routes of administration-intravenous, intramuscular, or spinal routes
Compare the mechanisms of action, drug effects, indications, adverse effects, cautions, contraindications, drug-drug and drug-food interactions, dosages, and routes of administration for nonnarcotic.
action-blocks peripheral pain impulses by inhibition of prostaglandin synthesis, also lowers febrile body temp by acting on the hypothalamus

indications,-treatment of mild to moderate pain and fever.

adverse effects-relatively safe drug, rash nausea, and vomiting, blood disorders, dyscarsias, nephrotoxicities.

contraindications-known drug allergy, severe liver diseased, genetic disesase known as glucose-6-phosphate dehydrogenase dificiency

drug-drug-Alcohol

routes of administration-PO