NUR 119 Mod 2

1: Normal - No change

2: Very mild - Forgets object location

3: Mild (early confusion) -Decreased ability to function in work situation

4: Moderate - Unable to perform complex tasks

5: Moderately severe - Usually needs assistance for survival

6: Severe (dementia) - Forgets names of spouse/family/caregivers and details of their personal lives

7: Very severe - Unable to speak (5 words or less)

Improves memory loss by elevating Ach concentration

Life-threateing: hepatotoxicity

glaucoma

Tx: relieve tremors & rigidity

OD signs: Agranulocytosis, hemolytic anemia, thrombocytopenia, cardia dysrhythmisa, neroleptic malignant syndrome

OD action:

increase

Incurable dimentia

Degeneration of cholinergic neuron and deficiency oif acetylcholine

Nausea & vomiting

Premature ventricular contraction (PVCs)

Orthostatic hypotension

• Dyskinesia - involuntary movement
• of tongue and body

tachycardia

CNS stimulation

It is an antiparkinson dopaminergic drug.

It stimulates dopamine receptors.

It can be used alone or in combination with carbidopa-levodopa (Sinemet)

Tx involves both levadopa and cardopa to increase the dopamine beyond the blood/brain barrier.

cardopa inhibits the dopa decarboxylase enzyme, whioch would convert 99% of the levadopa to dopamin BEFORE it got to the brain. Use 1p cardopa to 10p levadopa.

Either to reduce the symptoms or replace the domamine deficit

Degenerative CNS disorder

Abnormalities in movement (bradykinesia), posture, tremor, joint and muscle

Rigidity

Destruction/degenerative changes in dopamine producing nerve cells

Decreased dopamine/increased acetylcholine

Can develop with long-term use of antipsychotics (pseudoparkinson's)

OD!!!

• IV: 5-10mg
• rpt @ 10-15min
• MAX 30mg

Anticonvulsant

2-3 wk steadyt state

3-4 wk therapeutic levels

Monitor for anemia

Drug of choice for less than 2 years

aka Depakote - for grand, petit & psychoM

Tx neuropathy

Alcohol WD and anxiety.

Can be used for status epilepticus, but valium is choice there

drug of choice for status epilepticus

Barbituate-like drug for grand mal & psychomotor seizures

Anticonvulsant to control seizures in toxemia of pregnancy caused by eclampsia and preeclampsia

Anticonvulsant for grand mal seizures

Abrupt WD -> seizures

anticonvulsant to Tx facial pain assoc w/ triginmenial neural

Long term oral: Dilantin

CNS depression

Contraindicated for renal or liver damage

May cause bone marroe suppression

Dilantin will precipitate in D5W - use only 0.9 NS

hydantoin (Dilantin)

Oldest & most widely used

Also Tx cardiac arythmias

T1/2 18-24 hr (Maddie)

Steady Sate 7-21 days

TSR 10-20 mcg/mL

• May cause drowsiness
• Shake oral suspensons well

Correct the underlying cause

• Dilantin
• - T1/2 18-24 hr
• - Steady state 7-21 days
• - TDM 10-20 mcg/mL

If Pt stops dilantin for 2 weeks, seizures may resume

Need loading dose

Stop (but not cure) seizure w/ Valium & Ativan

Low blood sugar

Fever

Check PO₂

WD of drugs: cocain, lidocain, lithium, theophyline

3-5 days after alcohol WD

Complex symptoms: automatisms (repetitive behavior such as chewing or swallowing motions), behavioral changes, and motor seizures

Also called petit mal seizure; brief loss of consciousness lasting less than 10 seconds; fewer than three spike waves on the electroencephalogram (EEG) printout; usually occurs in children

Also called grand mal seizure; most common form of seizure. In the tonic phase, skeletal muscles contract or tighten in a spasm lasting 3 to 5 seconds. In the clonic phase, there is a dysrhythmic muscular contraction, or jerkiness, of legs and arms lasting 2 to 4 minutes.

Dysrhythmic muscle contraction

Sustained muscle contraction

Convulsive and nonconvulsive; involve both cerebral hemispheres of the brain

1. Administer an emetic, and follow with activated charcoal if the client is conscious; use gastric lavage if the client is unconscious.

2. Administer the benzodiazepine antagonist flumazenil(Romazicon) IV if required.

3. Maintain an airway, give oxygen as needed for decreased respirations, and monitor vital signs.

4. Give IV vasopressors for severe hypotension.

5. Request a mental health consultation for the client.

9 months after symptoms 1st appear

5 years after 2nd

long-term after 3rd

Involuntary paroxysmal mucle contractions.

The word paroxysm means "sudden attack, outburst".

Abnormal electrical discharges of the cerebral neurons and is characterized by a loss or disturbance of conciousness

• IV: 0.4 to 2 mg
• may repeat q2-3min
• max 10mg

• IV: 0.2 mg over 30 sec
• may repeat with 0.3 mg in 30 sec
• max: 3 mg total dose

• Benzodiazepine Antagonists
• (OD antidote)

PO: 10 to 30 mg q4h PRN

SR: 15 to 30 mg, q8-12h PRN

IV/IM/subQ: 2.5 to 15 mg q2 to 6h PRN

Epidural: 2 to 10 mg over 24h


SR=sustained release

PO: 325 to 650 mg q4-6h PRN; max: 4000 mg/d

Rectal supp: 650 mg q.i.d.

• Analgesic:
• PO: 325 to 650 mg q4h prn; max: 4 g/d

• TIA and thromboemboliccondition:
• PO: 81 to 325 mg/d

• Arthritis:
• PO: 3.6 to 5.4 g/d in divided doses

TDM: 15 to 30 mg/dL; 150 to 300 mcg/mL

• Symptoms:
• - CNS depression
• - Cardiovascular collapse

• Tx:
• - Airway
• - Charcoal
• - Fluids
• - EKG monitoring
• - Antiseizure meds

• Symptoms:
• - Adrenergic

• Tx:
• - Diuretics
• - Acidify urine
• - Hemodialysis

• Symptoms:
• - Agitation
• - Seizures

• Tx:
• - Supportive
• - Charcoal
• - anti-seizure meds

• Symptoms:
• - Altered levels of consciousness
• - Hallucinations
• - Convulsions (seizure)
• - Diminished urine output
• - Low Na⁺ (Na/K pump shot)
• - Oliguria
• - Coma
• - Death

• Tx:
• - Supportive
• - Fluid and electrolyte correction
• - Hemodialysis

• Symptoms:
• - CNS stimulation

• Tx:
• - Airway & charcoal

No becauseof the possible sewrios side effects.

Tofranil

Lithium

anticonvulsants

Wellbuitrin

Effexor

Prozac

Marplan

Nardil

Parnate

Tricyclic Antidepressants

Serotonin Reuptake Inhibitors

MAO's

Miscellanous

Mood Stabilizing

Depression

• 1) Reactive
• - loss of loved one
• - possible benzodiazepine

• 2) Major
• - loss of interest in work/home
• - inability to complete tasks
• - may be primary or secondary to physical or psychiatric problem
• - antidepressants

• 3) Bipolar affective disorder
• - manic (euphoric) or depressive (dysphoria)
• - Originally lithium, now depakote

Pt is beginnign ti suffer from the EPS of akathesia and pseudoparkinsonism.

Protrusion and rolling of the tongue

Sucking and smacking movements of the lips

Chewing motion

Facial dyskinesia

Involuntary movements of the body and extremities

Facial grimacing

Involuntary upward eye movement

Muscle spasms of the tongue, face, neck,and back (back muscle spasms cause 'trunk to arch forward)

Laryngeal spasms

Restless

Trouble standing still

Paces the floor

Feet in constant motion, rocking back and forth

Stooped posture

Shuffling gait

Rigidity

Bradykinesia

Tremors at rest

Pill-rolling motion of the hand

• Pseudoparkinsonism
• Akathisia
• Acute dystonia
• Tardive dyskinesia

Anticholinergic drugs help decrease:

pseudoparkinsonism symptoms

acute dystonia - benztropine (Cogentin)

akathisia - lorezepam

BUT has little effect on tardive dyskinesia, which means that the antipsychotic should be stopped for this adverse affect. Other drugs (benzodiazepines, clozapine) have been helpful for some Pt.

Pseudoparkinsonism:

Stooped posture

Shuffling gait

Rigidity

Bradykinesia

Tremors at rest

Pill-rolling motion of the hand

(Parkingson's disease affects the extrapyramydal motor tract of nerves)

Perhaps a lifetime.

• Haldol
• Zyprexa
• Risperdal

• thorazine
• prolixin
• stelazine (not in our book)

I only saw 1 - a dose of 0.5-5mg instead of 10-25mg.

antipsychotic drug

They block the action of the neurotransmitter dopamine and thus may be classified as dopaminergic antagonists.

All antipsychotics block the D₂ recepter, which in turn promotes the presense of EPS (extrapyramidal symptoms) resulting in pseudoparkinsonism.

Atypicals have a weak affinity for D₂, but a strong affinity for D₄ and they block the serotonine. These cause fewer EPS than typical (phenothiazines)

Thorazine (1952)

typical (or traditional)

atypical

a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness

It is losing contact with reality.

• Positive symptoms:
• incoherent speech
• hallucinations
• delusions
• paranoia

• Negative symptoms:
• poverty of speech
• social withdrawal
• poor self-cate

Restoril

flumazenil (Romazicon)

Generalize muscle weakness that may affect diaphram and intercostal muscles.

Caused by inadequate dosing of AChE inhibitors

Tx: neostigmine, a fast-acting AChE inhibitor, but an OD of this can lead to cholinergic crisiis, an exaccerbation of the same symptoms!!!!

Chronic autoimmune neuro-muscular disease

• Mostly:
• women < 30
• men > 50

• Cause:
• lack of ACh receptor sites.

Dolobid

Motrin

naproxen (Naprosyn)

Toradol - IM/IV: 30mg q6h; max 120 mg/d

Celebrex

tramadol

Toxic levels > 50 mcg/mLProbably hepatotoxic: > 200 mcg/mL

Early symptoms: nausea, vomiting , diarrhea and abdominal pain.

Death could occur in 1-4 days from hepatic necrosis.

Antidote: Mucomyst

Theraputic level: 5-20 mcg/mL

Toxic levels > 50 mcg/mL

Probably hepatotoxic: > 200 mcg/mL

4 g/d, unless taken regularly then it is suggested that the limit be 2 g/d.

No GI bleeding, nasea or vomiting

Does not interfere w/ blood clotting, nor does it pose a rsk of excessive bleeding for dysmenorrhea as does ASA/NSAID

Met-liver, ex-urine

Peak: 30-120 minutes

PO, Supp, IV

Is a third type of antiinflammatory drug after NSAIDs & corticosteroids.

Is a DMARD disease-modifying antirheumatoc drug that can be used although it is more toxic.

A chrysotheraoy or heavy metal therapy o which Auranofin is the most often used.

It is for sever arthristis.

Tylenol (acetaminophen)

Mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, tinnitus, and dizziness.

Severe poisonings and include hyperthermia, tachypnea, respiratory alkalosis, metabolic acidosis, hypokalemia, hypoglycemia, hallucinations, confusion, seizure, cerebral edema, and coma.

The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.

2-3 L per day

Anticoagulants

Steroids

Codein hydrocodone (oxycontin)

Alcohol

Ascorbic Acid

Suction NG tube & add charcoal.

If no NG tube -> quinton catheter (dialysis)

Large doses reequired for arthritis risk GI bleeds, i.e. theraputic blood levels 150-300 ug/mL (or 15-30 mg/dL)

6 of the 7 groups of NSAIDs all inhibit the COX-1 enzyme which provides protection for the stomach lining and so for sever arthritis: peptic ulcer and gastric bleeding

Selective COX-2 inhibitors (2 more than 1, but not 0) such as celecoxib (Celebrex) are good, but have other adverse reactions: peripheral edema.

Hypersensitivity to salicylates or NSAIDs

for no reason including fever in children 12 or younger

third trimester

Caution: renal or hepatic disorders & may cause bleeding, esp of GI

Analgesia

TIA (transient ischemic attack "small stroke") & Thromboembolic

Arthritis

She had this in with other analgesics, non of which were anti-inflammatory???

Indocin (an NSAID) with:

Potent antiinflammatory effects &

Graeter incidence of adverse effects.

NSAIDs

They work by inactivation of the cyclooxygenase (PTGS) enzyme required for prostaglandin and thromboxane synthesis.

But aspirin is different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors.

ASA or aspirin

Inhibit "prostaglandins"

Note #1 - suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (PTGS) enzyme required for prostaglandin and thromboxane synthesis

Note #2 - Prostaglandins are not endocrine hormones, but autocrine or paracrine, which are locally acting messenger molecules. They differ from hormones in that they are not produced at a discrete site but in many places throughout the human body. Also, their target cells are present in the immediate vicinity of the site of their secretion (of which there are many).

Note #3 - some actions:

cause constriction or dilation in vascular smooth muscle cells

cause aggregation or disaggregation of platelets

sensitize spinal neurons to pain

induce labor

decrease intraocular pressure

regulate inflammatory mediation

regulate calcium movement

control hormone regulation

control cell growth

acts on thermoregulatory center of hypothalamus to produce fever

acts on mesangial cells in the glomerulus of the kidney to increase glomerular filtration rate

acts on parietal cells in the stomach wall to inhibit acid secretion

CNS depressants

Anti-hypertensive drugs

MAOI - calming drugs

Pain is subjective

Morphine is a non-ceiling drug

Demerol is a ceiling drug - no more than 600mg/24hr and for no longer than 48-72 hrs

Use least potent analgesic when more than one is ordered.

Alternate narcotic with non-narcotic (xanax: anti-anxiety) for best pain relief

PO prefered for long-rterm use

Dosage should provide good pain relief (down to 3) w/o unacceptable adverse reactions.

Prompt admin and on regular sched

Other drugs for Pr comfort (laxatives, antidepressants, anyiemetics)

No high bu it occupies the receptors which alleviates the eithdrawal symptions of:

• diarrhea
• abdominal cramps
• restlessness
• watery eyes
• runny nose
• nasea

Disulfiram is a drug discovered in the 1920s and used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol.

NARCAN

REVEX

TREXAN

REVIA - 3-5x more potent than Narcan, not an antidote, Tx after off opioids 7 days

Observe all for signs of analgesic reversal: tachycardia, nausea, vomiting & sweating.

Additional observation of rnarcan: bleeding resulting from an elevated partial thromboplastin time.

1) Opioid overdose or post-op respiratory depression.

2) Respiratory depression in neonates resulting from maternal opioid use.

Antidotes for overdoses of natural or synthetic opioids.

Higher affinity for the opioid receptors, so it blocks and displaces resulting inthe inhibition of an opioid action.

Buprenex

Stadol

Nubain

Talwin

Nalbuphine

They are combinations of opioid antagonists (Narcan) added to opioid agonists in hopes of decreasing opioid abuse, i.e. a lower potential for dependence.

Codeine

Vicodin

Dilaudid

Demerol

OxyContin

Percocet

Percodan

Methadone

1/15 to 1/20th as potent

meperidine (Demerol)

Asthma with respiratory depression

Increased intracranial prewssure

Shock

Caution: respiratory, renal, hepatic diseases, MI, old & young

Indications: Pain from

Acute Myocardial Infarction (AMI)

Cancer

Dysnea from pulmonary edema

Preoperative medication

12 hours

• Peak:
• IV = 10-20 min
• IM = 30 min
• SQ = 60-90 min

PO as Roxanol & MSContin

• Other routes:
• Epidural - space within the canal (formed by the surrounding vertebrae) lying outside the dura mater
• Intrathecal - space under the arachnoid membrane of the brain or spinal cord

Met-liver ex-kidney

Hydromorphone (Dilaudid)

semisynthetic opioid

6X analgesia over morphine

fewer hypnotic effects

less GI distress

faster onset

shorter duration

life-threatening Respiratory depression

Nasea & Vomiting

Pupil Contraction: 3-7 normal, 1=narcotic

seizures (CNS)

Slowed GI motility

Muscle Spasms in bowel & billiary (bile) tract

life-threatening increased intracranial pressure

Hypotension

Urinary retention

urticaria (hives)

Morphine

Reduce the perception of pain

Produce sedation

Suppress cough

Lower BP

Decrease emotional upset

Most are Schedule II.

The body's enforphins, though not well understood, activate the same receptors as opioids.

Superficial (skin & mucous membranes) or somatic (skeletal muscles ligaments & joints) are via the sympathetic NS and can increase BP and P.

Deep (visceral) pain from smooth muscles and organs is parasympathetic (the innervation type) and can lower BP to the point of syncopy.

Close large diameter (neuro) fibers.

<= 3

Acute pain is trasnmitted via A delta fibers, which are myelinated and result in a rapid transmission of pain.

Chronic or dull pain is more often associated with unmyelinated C fibers. Chronic pain lasts longer than 3 months - Maddie.

By origin: Nociceptors (sensory pain receptors, i.e. in tissues, bones, muscles or visceral - organ) are activated by noxious stimuli (mechanical, thermal or chemical) in peripheral tissues.

Neuropathic pain results from damage or diseasy to the PNS or CNS - burning, tingling or electrical shocks, often caused by a light touch.

Histamines, Bradykinins and Prostraglandins are chemically involved in the transmission of pain signals.

Oxygen - lack of results in CNS depression

Normal PO₂ is 95-100, but may be as low as 92 for a COPD Pt.

Glucose - Too much insulin leads to coma

Thiamine - Deficiency causes degradation of myelin sheath reducing glucose by 1/2

Excess Norepinephrine

Increased Excitatory receptors

Decreased Inhibitory receptors

Increased Sensitivity of excitatory receptors

Decreased Sensitivity of inhibitory receptors

Decreased GABA

BOTH EXCITATORY & INHIBITORY

INHIBITORY

Think turkey - tryptophan from which it is derived - it inhibits CNS

EXCITATORY or INHIBITORY

Mostly sympathetic via norepinephrine

USES GABA-INHIBITORY

Major inhibatory neurotransmitter

Not enough GABA (gamma-Aminobutyric acid) causes anxiety, hyper-arrousal, seizures.

EXCITATORY or INHIBITORY

dopamine agonists stimulate the dopamine receptors

Parkinsons (shuffling gate, intention tremor) is the destruction of the dopamine neurons

Excitatory or INHIBITORY

Memory, arrousal, speech

Low for Alzheimer's Pt, i.e. Acetylcholine

Treatment drug: donepezil (Aricept), which is an AChE (acetylecholinesterase inhibitor). AChE is the enzyme that breaks down ACh. If you inhibit that enzyme, you get more ACh by virtue of it not being broken down.

Many fucntions, but chiefly protection. Myelin sheath are Schwann cells - a type if glial cell.

depression

Makes it nonresponsive

increases excitability

Amino acids from food to create them?

Oxygen & insulin?

Large Molecule

ACTH - Corticosteroids release in resp to biological stress

ADH - Low BP

• Amino Acids
• Inhibitor

• Amines
• Excite

• Small molecule
• Inhibitor
• Parasympathetic

Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse.

Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane in the axon terminal, on the presynaptic side of a synapse.

They are released into and diffuse across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.

• A. Long
• B. Short

• A. Short
• B. Long

• A. Craniosacral division
• B. Preganglioic fibers
• C. Cranial (III, VII, IX and X)
• D. Sacral (S2, S3 and S4)

• A. thoraco-lumbar
• B. preganglioic fibers
• C. thoracic (T1 - T12)
• D. Lumbar (L1 & L2)

• A. Excitability
• B. Inhibition

• A. Sympathetic
• B. Parasympathetic
• C. Opposite

• A. Cholinergic system
• B. Acetylcholine

• A. adrenergic system
• B. norepinephrine

• A. Sympathetic
• B. Parasympathetic

• A. involunrtary
• B. Visceral system
• C. Heart
• D. respiratory system
• E. gastrointestonal system
• F. Glands

• A. Volutary
• B. Skeletal muscles
• C. Respiratory muscles

Somatic (SNS) & Autonomic (ANS) nervous systems

CNS & PNS

Increase or block nerve (neuron) call activity.

Brain & Spinal cord

• Preg Cat X for ergot alkaloids
• C for all triptans

• Imitrex
• Amerge
• Maxalt
• Zomig - Avoid for uncontrolled hypertension, IHD (ischemic heart dis) or prior MI

• Axert
• Frova
• Relpax

No aspirin because of the risk of Reye syndrome -> neurologic prolems assoc w/ viral infects treated with salicylates.

Usze acetaminophen (Tylenol) instead.

Patho: inflammation and dilation of cranial vessels.

Etiological theory: neurotransmitter serotonin imbalance, which normally cause vasoconstriction to suppress migrains.

Triptans are selective serotonin receptor agonists, i.e. they facilitate whatever serotonin present to do what it normally does - cause vasoconstriction.

1) Preventative, e.g. beta andrenergic blockers like propanolol (Inderal)

2) Mild migrain attacks: aspirin thru demerol

3) Triptans are better than ergot alkaloids for acute migrains.

Increased fluid intake and especially alkaline urine, since low pH which precipitates the uric acid into crystals which collect in joints and in kidneys as stones.

Effective in alleviating chronic gout, but they should not be used during acute attacks.

Probenecid can be taken with colchicine.

Initially w/ small doses of colchicine should be given before adding probenecid.

If gastric irritation occurs, probenecid should be taken with meals.

T1/2 8 to 10 hours

85% to 95% protein-bound. Use caution when administering this drug with other highly protein-bound drugs.

Probenecid blocks the renal reabsorption of uric acid.

It can be used to treat chronic gout with colchicine, etc., but should not be used for acute attacks.

Acute treatment include nonsteroidal antiinflammatory drugs (NSAIDs), colchicine and steroids.

While indomethacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.

Uric acid > 6 mg/dL for women and 6.8 mg/dL for men.

Uric acid is not very soluable, so it crystallizes in the blood and then collects on joints - gouty arthritis.

Allopurinol (Zyloprim) is a uric acid biosynthesys inhibitor that works by inhibiting the enzyme xanthine oxidase which is needed for the synthesis of uric acid. It is a preventative (prophylactic) measure.

Uricosurics like probenecid (Benemid) increase the rate of uric acid excresion by inhibiting its reabsorption by the kidneys, but shouylf not be used for acute gout.

colchicine (Colcrys) is effective at decreasing acute gout symptoms (inflammation), but not at treating gout as the above 2 do.

Pt may well have a physical or phychological dependence and may very well have developed a tolerance as evidenced by her taking twice the normal dose. Pt should have been instructed not to consume alchhol with this drug because the combination could result in excessive sedation.

• Dalmane
• Restoril
• Halcion

• Xanax
• Librium
• Klonopin
• Valium
• Ativan
• Versed

taper off

antiemetic

counteract...

Decreased:

occurrence of hangover

respiratory depression

Can be given to clients with mild liver dysfunction

Class of drug: Azapirones

Drug: buspirone HCl (BuSpar)

Class of drug: non-benzodiazepines

• Drug:
• Chloral Hydrate
• Ambien

flumazenil

It is a benzodiazepiene antagonist.

Hypersensitivity

CNS depression

shock

coma

narrow-ancle glaucoma

pregnancy

lactation

Caution: Hepatic or renal dysfunction, suicidal

gamma-aminonutyric acid (GABA), an inhibitory neurotransmitter within the CNS

Not meant for long-term use, e.g. > 4 months (Maddie: lose effectiveness after 4 weeks daily use.

Wide margin of safety between therapeutic and toxic dose

Lipid-soluble

May cause CNS depression (respiratory depression and excessive sedation)

Taper gradually to prevent withdrawal. May cause dependence

Metabloized - liver

Excreted - urine

Steady state- 5 to 7 days

Therapeutic in 2 to 3 days

Maddie: Should not be taken every night, but should be taken at bedtime.

alprazolam (Xanax)

chlordiazepoxide HCl (Librium)

clorazepate dipotassium (Tranxene)

diazepam (Valium)

lorazepam (Ativan)

oxazepam (Serax)

Class: Benzodiazapine

Generic: Lorazepam

Trade: Atavan

Insomnia is often defined as a positive response to:

Do you experience difficulty sleeping? or

Do you have difficulty falling or staying asleep?

Transient insomnia lasts for less than a week.

Acute < 1 month, or chronic

Primary and secondary

Primary anxiety is not caused by a medical condition or by drug use

Secondary anxiety is related to selected drug use or medical or psychiatric disorders.

Anxiolytics are not usually given for secondary anxiety unless the medical problem is untreatable, severe, and causes disability. In this case an, anxiolytic could be given for a short period to alleviate any acute anxiety attacks.

These agents treat the symptoms but do not cure them.

Long-term use of anxiolytics is discouraged, because tolerance develops within weeks or months depending on the agent. Drug tolerance can occur in less than 2 to 3 months in clients who take meprobamate or phenobarbital.

Antianxiety drugs, used primarily to treat anxiety and insomia.