1. Stimulate Bladder w/urinary retention or atonic bladder
2. Increases GI tone, salivation & GI and Bronchial secretions
3. Constricts pupils in patients w/glaucoma
4. Increases neuromuscular transmission
5. Decreases h/r and bp

decreases pulse and BP through vasodilation

slows conduction of AV node

increase smooth muscle tone and motility

increase peristalsis

relax sphincter muscles

increases secretions

contracts bladder muscles

stimulate urination

increases ureter tone

relax sphincter muscles

increases pupil constriction (miosis)

increase accomodation vision (near/far)

lacrimation (tears)

bronchial smooth muscle contraction/constriction

increase bronchial secretions

They are named after the specific chemicals that bind to them

Muscarinic: named after the alkoloid muscarine

Nicotinic: named after the alkoloid nicotine

Affect smooth muscles located in CNS, heart & glands

Slows heart rate

Response is generally inhibitory except stimulation of glandular secretions

affect skeletal muscles

response is mostely excitatory

• Also known as parasympathomimetics, cholinomimetics, cholinergic stimulants, cholinergic agonists

• Mimic parasympathetic neurotransmitter acetylcholine (Ach) located @ the ganglions & the parasympathetic terminal nerve endings

• Innervates the receptors in organs, tissues, and glands

• Also called muscarinic agonists
• Selective to muscarinic receptors
• Enhance the PNS activity of 'rest and digest'
• Receptors are located in smooth muscle-activate tissue response: Heart, GI, GU, glands
• Relatively resistant to the destructive effects of the enzyme acetylcholinesterase which destroys endogenous Ach.

• Hypotension, bradycardia
• Blurred vision, miosis
• Excessive salivation, sweating, increased gastric acid, N/V/D, abdominal cramps
• Bronchoconstriction

1. Monitor BP/P, teach client to arise slowly
2. Record fluid intake and output
3. Monitor breath and bowel sounds
4. Give 1 hour before or 2 hours after meals
5. Monitor for overdosing:

• S&S: salivation, sweating, flushing, abd cramps
• Antidote: atropine

Ach is normally synthesized in the presynaptic nerve terminals from choline and acetyl coenzyme

Stored in vesicles in the presynaptic neuron

When the neuron is stimulated, Ach is released into the cleft then diffuses across to the receptors in the peripheral nerves as well as central nerves

Ach reacts w/target cells to stimulate skeletal muscles

Ach in the synaptic cleft is rapidly destroyed by the enzyme AchE (stopping its actions) and degrades Ach into choline and acetate group; the choline is taken up by the presynaptic neuron and reused to make more Ach- and the cycle is repeated

They are also called cholinesterase inhibitors/blockers, acetylcholinesterase (AchE) inhibitors, or anticholinesterases

Do not act directly on receptors, are nonselective and affect all Ach sites:

• autonomic ganglia, muscarinic receptors, skeletal muscle, and Ach sites in the CNS

• Break down cholinesterase enzyme into choline and acetic acid

• Prevents the destruction of endogenous Ach so it remains on the cholinergic receptors longer which prolongs its action

• Allow Ach to activate muscarinic and nicotinic cholinergic receptors

Effects: nonselective-good and bad

• Stimulate skeletal muscles, increase tone
• Incrased GI motility, bradycardia, miosis
• Bronchial constriction, promote urination

Side Effects: bradycardia, asthma, peptic ulcers

Contraindications: intestinal and urinary obstruction

-Produce pupil constriction in glaucoma
-Increase bladder tone

-Increase muscle strength in myasthenia gravis

• neostigmine (Prostigmin): short acting
• pyridostigmine (Mestinon): moderate acting
• edrophonium (Tensilon): immediate acting for dx purposes

-donepezil (Aricept), tacrine (Cognex) for Alheimer's patients
-Antidote to anticholinergic drugs, TCAs, opiods

Muscle cramps, twitching, bradycardia, increase bronchial secretions

Cautions: patients w/bradycardia, arrythmias, asthma, peptic ulcers, hypothyroidism, intestinal and urinary obstructions.

indirect acting cholinergic drug that binds the enzyme cholinesterase permanently; potent, long lasting effects

Cholinesterase must be regenerated before the drug efffect diminishes and can take days to weeks

Produce pupillary constriction

Manufacturing of insecticides

Potent neurotoxins- excessive salivation, eye-watering, muscle spasms and death

ie: snake venoms, nerve gases (Sarin)

Antidote: pralidoxime

Side effects: due to increased cholinergic stimulation- slaivation, sweating, flushing, head ache, abdominal cramps

Contraindications: patients w/possible GI or urinary obstructions

Also known as: parasympatholytics, cholinergic blocking agents, cholinergic/muscarinic antagonists, antiparasympathetic agents, and antimuscarinic agents

Anticholinergic and adrenergic drugs produce many of the same responses

Inhibit the actions of Ach by occupying the Ach muscarinic receptors; therefore permit the adrenergic (SNS) effects to dominate

GI: rela smooth muscle tone, decrease motility, peristalsis and spasms, decrease acid secretion

GU: relax detrusor muscle (allowing it to fill with urine), increase sphincter constriction

1. Useful in emergency CV situations; increases pulse w/bradycardia

2. Useful as a preop med- decreases salivary & respiratory secretions

3. Antispasmodic: (Probanthine) treat peptic ulcers by relaxing smooth muscles of GI tract and decreases motility/peristalis; treats irritable bowel syndrome

4. Useful w/eye exam: paralyzes ciliary muscles

5. Antidote for muscarinic agonist overdose/poisoning

Well absorbed IV and po w/onset 30-60 onset

has a short half life

Side effects: tachycardia, palpitations, nasal congestion, flushing, photophobia, blurred vision, dry mouth, skin and eyes, decrease perspiration, head ache, nausea, abd distention, urinary retention, constipation, impotence, and coma

Contraindications: patients w/glaucoma, urinary or GI tract obstruction, COPD, severe ulcerative colitis, unstable CV status, MG

• Monitor vital signs, urine output, bowel sounds
• Safety: use bedside rails, caution against driving vehicles
• Provide mouth care and eye drops
• Avoid hot environments
• Avoid alcohol, cigarettes, caffeine, and aspirin at bedtimes
• Warn to wear sunglasses in bright light

benztropine (Cogentin)

trihexyphenidyl HCl (Artane)

Action: decrease involuntary movement, termors, muscle rigidity

Side effects: eimilar to anticholinergics

Use: Parkinsons and Pseudoparkinsonism

Composed of brain and spinal cord

Regulates body functions

Relays messages

Processes, compares and interprets information sent by impulses from the peripheral nervous system and returns the instruction through the PNS for apporpraite cellular actions

Acetylcholine (Ach): is inactivated by the enzyme cholinesterase

Norepinephrine (NE): inactivated by reuptake or by the enzymes COMT or MAO

Serotonin (S): inactived by reuptake & MAO breakdown

Dopamine (D): inactived by reuptake or by COMT or MAO

Gaba: inactivated by enzyme breakdown

Increases neurotransmitter levels in CNS:

-increases neuronal discharge

-blocks an inhibitory neurotransmitter

Highly addictive

can produce psychologic dependence or tolerance

Must gradually increase dose when beginning therapy

Do not abruptly stop these drugs as this could lead to depression and withdrawal symptoms

Amphetamines- stimulate cerebral cortex of the brain

Analeptics (caffeine)- stimulate respirations

Anorexiants- suppress appetite

ADHD

Narcolepsy

Reversal of respiratory distress

Obesity

dysregulation of transmitters S, NE, D in reticular activating system of the brain

Unclear

May be asociated w/high levels of lead in childhood, prenatal exposure to alcohol, and drugs

May be genetic factors w/environmental ties

May be a deficit of, or dysfunction of D, NE, or S in the reticular activating system of the brain

~5% of all children

Occurs primarily in children before 7

3-8x more likely in boys

Usually more overt in boys

• Recurrent attacks of drowsiness and sleep during daytime
• Brief, involuntary episodes of falling asleep while driving, talking, eating, standing
• Unable to control sleep
• Abnormality in REM sleep
• Has a hereditry component; type of autoimmune disorder

CNS stimulants: stimulate release of NE and D from brain and SNS nerve terminals

ordinarily cause euphoria and alertness, termors, and irritablity

• Increase wakefulness in narcolepsy
• Increase attention span, cognition
• Decrease hyperactivity, impulsiveness, restlessness of ADHD:

- stimulate specific areas of CNS that heighten alertness & increase focus

- reverse many of the symptoms of ADHD and help patient better focus on tasks

Uses: ADHD, fatigue, narcolepsy

Given twice daily (morning/early afternoon)

30-45 min before meals; well absorbed from GI tract

1/2 life 1-3 hours, excreted in urine

Action: acts on cerebral cortex, reticular activity system

• Caffeine may increase effects
• Decreases effects of decongestants, hyperintensives, barbiturates
• May alter effects of insulin
• Increases elffects of PO anticoagulants, anticonvulsants, TCAs

tachycardia, palpitations, dizziness, hypertension

sleeplessness, restlessness, nervousness, tremors, irritability

increased hyperactivity

anoreia, dry mouth, V/D, weight loss

hepatotoxicity

thrombocytopenia

• Give before breakfast and by early afternoon
• report irregular heart beat
• record height, weight, and growth of children
• avoid alcohol, caffeine
• use sugarless gum to relieve dry mouth
• do not stop abruptly, taper off instead
• counseling must be utilized
• periodic drug holidays may be necessary to decrease dependence and to assess drug benefits or side effects

very tight muscles of head and neck; etiology usually stress

Annyoing, steady lingering pain; generally self limiting

usually treated with OTCs: ASA, acetaminophen, ibuprofen

Unilateral throbbing or pulsating pain disrupting ADLs

Associated w/aura, N/V, photophobia

Caused by inflammation and diation of blood vessels in head

Triggers: nitrates, cheese, chocolate, red wine, food additives, caffeine, MSG, perfumes

Lasts for hours or days

Usually affects females in their 20s and 30s

May result from imbalance of serotonin that cuases vasoconstriction and suppresses migraines

Severe unilateral non-throbbing pain

Usually located around the eye

Occurs in series of attacks

More common in men

administer:

beta-adrenergic blockers

calcium channel blockers

anticonvulsants: valproic acid

tricyclic antideppressants

all have the potential to produce se; therefore not ideal unless the only option to prevent migraines

A serotonin receptor agonist

- serotonin receptors found throught the CNS, CV, and GI systems

Used in the management of migraine and cluster headaches

Action: causes vasoconstriction of cranial arteries therefore inhibiting and reducing the inflammatory process along the trigeminal nerve pathway

Use: treat migraine or cluster headaches

dizziness, tingling, numbness, warm sensation, drowsiness, seizures

muscle cramps, N/V/D

dysrhythmias, thomboembolus, heart attack, stroke

Cause varying degrees of depression w/in CNS

Degree of depression depends primarily on the drug & amount taken

Create a continuum from relaxation to sedation to induction of sleep to anesthesia, to coma, and even death

Broad classification: sedative-hypnotics, general and local anesthetics, analgesics, narcotic, and non-narcotic analgesics, anticonvulsants, antipsychotics, and anti depressants.

Sedation: mildest form of CNS depression

used mostly during the daytime, to relax and sedate a person

diminishes physical/mental responses @ lower dosages

do not affect consciousness

Hypnotic effect: used to induce sleep, one of the most frequently prescribed drugs

Sedative-hypnotics: sometimes the same drug but given at higher doses as a hypnotic; anesthesia may be achieved with very high doses

Short-acting: useful for achieving sleep; allow person to awaken w/out lingering side effects

Intermediate-acting: useful for sustaining sleep; may have residual drowsiness in the morning

Residual drowsiness

REM rebound

Drug dependence

Drug tolerance

Excessive depression

Respiratory distress/depression

Withdrawal symptoms

Should be used short-term basis to prevent drug dependence, tolerance, and rebound insomnia

Low dose: decrease anxiety and promote drowsiness

Mod dose: inhibit seizure activity and promote sleep

High dose: anesthetic effects

Drug-drug: cuation w/alcohol, narcotics, other sedative-hypnotics as they have additive CNS depressive effects

used as general anesthetic

Use: induce sleep; rapid onset, short duration; no residual drowsiness

Side effects: hangover, dizziness, paradoxical excitement in elderly, respiratory distress, laryngospasm

Interactions: decreased respirations w/alcohol, CNS depressants, and MAOI's

Intermediate-acting:

Induce and sustain sleep

Onset ~ 1hour

Residual drowsiness (hangover effect)

Long-acting:

used to control seizures

ie: phenobarbital

Assess:

renal function

withdrawal symptoms-can be life-threatening; seizures/psychosis

tolerance

abuse

A benzodiazepine as hypnotics used to reduce anxiety and treat insomnia; may result in vivid dreams

Side effects: additive depressive CNS response if taken w/alcohol or narcotics; tolerance, respiratory depression, termors, ataxia, drug dependence, drowsiness, dizziness, confusion, weakness, fainting, head ache

Drug-drug: digitalis, phenobarbital

Decreased doses recommended w/renal or hepatic dysfunction and for older adults

• More likely to experience medication related sleep problems
• Barbiturates increase CNS depression and confusion in older adults; so should not be taken for sleep
• Short to intermediate-acting benzos are considered safer than barbs

- best to not take every night to avoid side effects/dependence

• Avoid long-acting benzodiazepines- may seem to help the insomnia for a night or two; but can produce generalized brain dysfunction as the med accumulates in the system

First use nonpharmacologic methods

Take med 15-45 min before bed

Report hangover effect

Be attentive to safety

Avoid alcohol, other CNS depressants

Monitor BP, R, withdrawal symptoms

Monitor LOC, therapeutic blood levels

Do not abruptly discontinue

Goal: provide a repaid & complete loss of sensations throughout the entire body, accompanied by a loss of consciousness; depresses the CNS and alleviates pain

Purpose: analgesia, muscle relaxation, loss of consiousness, amnesia

Rarely achieved by one drug

Several theories about how inhalation anesthetics cause CNS depression and LOC

A combination of drugs; frequently used in general anesthesia

Decreases amount of general anesthesia needed and decreases possible side effects; quicker recovery

Minimizes CV and other organ system problems and dysfunction, decreases possible post anesthetic N/V

1. Analgesia (induction stage): begins w/consciousness, speech becomes difficulut, dreams, auditory & visual hallucinations may occur; loss of pain. Ends w/loss of consciousness

2. Excitement/hyperactivity/delirium stage: produces aloss of consciousness caused by cerebral cortex depression; may see confusion/excitement/delirium. P/R may become irregular, and BP ↑

3. Surgical stage: skeletal muscles relaxes; as anesthesia deepens, shallow respirations, increased respiratory rate but stabilizes w/time

4. Medullary paralysis/toxic stage: respirations are lost, circulatory collapse; need ventrilator assistance (want to avoid)

respiratory depression

hypotension

dysrhythmias

hepatic dysfunction

Monitor patient's level of consciousness

Monitor vitals: resp/cardio status

Monitor urine output

Administer analgesics as necessary

Tonic-clonic

Most common

Involves both cerebral hemisphees of brain

May be preceded by aura

Generalized alternating muscle spasms and jerkiness

Tonic: intense skeletal muscles contract in a spasm lasting 3-5 seconds; loss of consciousness, bowel and bladder control, shallow breathing or brief periods of apnea

Clonic: dysrhythmic muscular contraction/jerkiness of legs and arms lasting 2-4 minutes

Postictal state: 'post seizure' drowsiness, disorientation, period of deep sleep

brief loss of consciousness- 10 seconds or less

begins and ends abruptly

subtle symptoms: staring into space, eyelid fluttering, altered vision, myoclonic jerks

usually occurs in children

• involves one hemispher of the brain
• no loss of consciousness in simple (focal) partial seizures
• involves spontaneous movement that may spread
• usually begin in one area and may progress to another; can develop into a generalize seizure
• frequently preceded by aura

• loss of consciousness; usually starts with blank stare followed by random activity
• appears unaware of surroundings; may have confusion, memory impairment, incontinence
• may have bizarre behaviors: hallucinations, mentaldistortions, changes in personality, loss of social inhibitions
• may lead to generalized seizures
• frequently preceded by aura

1. Suppress Na+ influx across neuron membraine: Dilantin

2. Suppress Ca++ influx which ↓ nerve transmission in motor cortex & therefore ↑ seizure threshold & ↓ seizure activity: Valproic Acid

3. Enhance action of or inhibit degradation of GABA

• N/V, gingivitis, gingival hyperplasia
• Neurologic: headache, diplopia, nystagmus, dizziness, lethargy, slurred speech, decreased coordination (ataxia), alopecia
• Pink/red/brown colored urine
• Bleeding, thrombocytopenia (low platelet count), aplastic anemia, leukipenia (low WBC count)
• Can have hyperglycemia
• More likely to occur in the elderly

• competes w/other drugs for protein binding sites

• ↑ effects if given w/Tagamet, INH, sulfonamides (inhibit its metabolism in liver)

• ↓ effects when taken w/folic acid, antacids, calcium, carafate, antineoplastics, antipsychotics, primrose, ginkgo

• Variable effect (but usually increases) of ASA, anticoagulant

• ↓ oral contraceptives, antihistamines, dopamine, theophylline, corticosteroids

Narrow therapeutic range: 10-20 mcg/ml

Onset of action: 30 min - 2hrs; peaks 1.5-3 hours

Highly protein bound

1/2 life: ~22hrs, but can range 6-45hrs

Steady serum concentration 7-10 days

Non addicting: does not have abuse potential or CNS depression

for petit mal, grand mal, and mixed type seizures

acto on GABA

monitor liver enzymes (hepatotoxicity)

Side effects: sedation, drowsiness, hepatotoxcity

Direct-acting cholinergic:

For urinary retention- increases urination, increases peristalsis in GI tract (reflux esophagitis)

Contraindications: bradycardia, hypotension, COPD/asthma, peptic ulcer, parkinsonism, hypothyroidism, intestinal or UT obstructions, prostate enlargement

• Muscle rigidity: abnormally increased muscle tone, stiffness, may have difficulty bending over
• Bradykinesia: slow limited movement, weakness and difficulty chewing, swallowing, speaking
• Tremors of head/neck: "shaking palsy" hands, arms, & head develop a motion of shakiness; difficulty initiating movement & controlling fine muscle movements
• Postural changes: head/chest thrown forward
• Shuffling walk
• Lack of facial expression
• Pill-rolling motion of hands

• Block the action of ACh @ cholinergic receptors and therefore balance the abundance of ACh compared to the scarcity of DA; also helps to prolong the actions of any dopamine that is present

• Used early in the course of therapy & patients who cant tolerate levodopa

• Reduce the rigidity & some of the tremors

• Minimal effect on bradykinesia

• Side effects: dry mouth, blurred vision, tachycardia, sedation, drowsiness, dizziness, hypotension, urine retention, constipation

an inhibitory neurotransmitter; released from the dopaminergic neurons

normally maintains control of Ach (inhibits its excitatory response)

to reduce the symptoms and increase the ability to perform normal ADLs

minimize the dopamine deficit and restore the natural balance between dopamine and ACh

1:10 ratio of carbidopa to levodopa

Developed the inhibit the enzyme dopa decarboxylase in the peripheral nervous system so more levodopa reaches the brain

therefore, smaller doses of levodopa are required to achieve the desired effects

May take ~ 6 months to achieve max therapeutic effects

Side effects:

fatigue, insomnia, dry mouth, blurred vision, dizziness, HA

orthostatic hypotension, palpitations, dysrhythmias

urinary retention, anorexia, dysphagia, nausea, vomiting

dyskinesia, psychosis, severe depression, nightmares, mental disturbances, SI

Drug interactions:

decreased levodopa effect w/ anticholinergics, phenytoin, tricyclic antidepressants, MAO inhibitors, benzos, phenothiazines, vit B₆

• Loss of memory- becoming more and more severe, logical thinking, judgment, paranoia
• Time disorientation
• Personality changes, hositility, aggressive behavior
• Hyperactivity
• Tendancy to wander
• Inability to express oneself
• Inability to recognize family or friends

• Various causative theories: genetic predisposition, slow virus or infection that attacks brain cells
• Neuritic plaques form outside neurons in cerebral cortex
• Neurofibrillary tangles and twists inside neurons; chronic inflammatory or oxidative cellular damage to neurons
• Cholinergic neurotransmitter degeneration abnormality

Inhibits MAO-B, which prolongs the action of levodopa  because MAO-B enzyme causes the catabolims/breakdown of dopamine and causes an increased level of dopamine

May use to delay the need for levodopa therapy by a year

Avoid food shigh in tyramine (can cause hypertensive crisis)

Avoid various TCAs and SSRIs

used to improve cognitive/memory function

may slow the disease process, but short-lasting effect

short 1/2 life; absorbed faster in GI tract w/out food

hepatotoxicity may occur