nervous system

NERVOUS SYSTEM

NERVOUS SYSTEM

• Responsible for controlling human functions, stimulus analysis and integration of external and internal responses

• Two main divisions:• a. Central nervous system – brain, spinal cord• b. peripheral nervous system – sensory

receptors and motor nerves

• PHYSIOLOGY OF THE NERVOUS SYSTEMElectrical impulses and chemical messengers –

transmit information throughout the body

NEURONSParts Function

Soma/cell body cell nucleus, cytoplasm, granules

Dendrites short, branch-like projections that cover the most surface of neuron; brings information from one neuron to another

Axon Carries information from a nerve to be transmitted to effector cells – muscle, gland, another nerve (axon terminal)

ACTION POTENTIAL• Nerves send messages by conducting electrical impulses ->

action potentials• Send messages to effector cells NERVE SYNAPSE• When action potential reaches end of n axon -> impulse

comes to halt -> stimulus no longer travels at electrical speed• Transmission between two nerves or between nerve and

muscle/gland is chemical

SYNAPSE: communication between two nerves or effectors• : presynaptic nerve, synaptic cleft, postsynaptic nerves• Neurotransmitter is released

Acetylcholine Communicates between nerves and muscles

Norepinephrine and epinephrine

Catecholamines; brain and limbic system

Dopamine Brain; coordination of impulses and responses, both motor and intellectual

Gamma-aminobutyric acid (GABA)

Brain; inhibits nerve activity; prevents overexcitability or stimulation

Serotonin Limbic system; arousal and sleep; preventing depression and promoting motivation

• Many drugs affecting nervous system involve altering activity of the nerve synapse

• Drugs block reuptake of neurotransmitters -> present in the synapse in greater quantities and cause more reaction

• Block receptor sites -> cannot stimulate receptor sites

• Block enzymes that breakdown neurotransmitters• Stimulates specific receptor sites when the

neurotransmitter• Causes the presynaptic nerve to release greater

amounts of the neurotransmitter

DRUGS AFFECTING THE AUTONOMIC NERVOUS SYSTEM

SYMPATHETIC PARASYMPATHETIC

Major neurotransmitter

Catecholamines:-epinephrine, norepinephrine, dopamine

Acetylcholine (Ach)

Nerve endings Adrenergic fibers Cholinergic fibers

Receptor Alpha, beta, dopaminergic

Nicotinic, muscarinic

Response Fight and flight Rest and digest

Effects Increase v/s, decrease GI; vasoconstriction

Decrease v/s, increase GI; vasodilation

SYMPATHETIC PARASYMPATHETIC

ConstipationUrinary retentionMyadriasisBronchodilationRelaxation of musclesDry eyesDry mouth

DiarrheaUrinary incontinenceMiosisBronchoconstrictionExcitation of musclesLacrimationSalivation

FOUR GROUPS OF ANS MEDSDRUGS DESCRIPTION

Cholinergic agents

- medications that cause effects in the body similar to those produced by acetylcholine

- Parasympathomimetic agents- Mimic the action of parasympathetic

divisionAdrenergic agents - Medications that cause effects similar to

those produced by adrenergic neurotransmitter/catecholamines

- Sympathomimetic agents

Anticholinergic agents

- Block or inhibit cholinergic activity

Adrenergic blocking agents

- Inhibit adrenergic system/activity

ADRENERGIC AGENTS• Classification by chemical

• Classification by action

CATECHOLAMINES NON-CATECHOLAMINES

Body’s natural neurotransmitter Synthetically made

Norepinephrine, epinephrine, dopamine Similar to catecholamines

Fast-acting More selective to types of receptors

Longer duration of action

Direct-acting Acts directly on the organ/tissue innervated by the SNS

Indirect-acting Triggers release of neurotransmitter (NE)

Dual-acting Both direct and indirect actions

RECEPTORS OF THE AUTONOMIC NERVOUS SYSTEM

• Alpha (α)

• Beta (β)

• Dopaminergic - improves symptoms associated with Parkinson’s

disease

alpha-1 receptors vasoconstriction of blood vessels

alpha-2 receptors mediator of negative feedback; preventing release of norepinephrine

beta-1 receptors

(heart) Increase in HR, increase contractility, stimulates vasoconstrictions

Beta-2 receptors (lungs) Relaxation of smooth muscles in the bronchi (dilation), uterus (relaxation) peripheral arterial blood vessels (vasodilation)

MECHANISM OF ACTIONS :• stimulate alpha and beta adrenergic receptor

directly or trigger the release of catecholamines indirectly causing sympathetic effects.

PHARMACOKINETICS:• A - can’t be taken by mouth or SL; SQ – slow ->

blood vessels constrict• D – widely distributed• M – predominantly in the liver; GIT, lungs,

kidneys, plasma, other tissues• E – primarily urine

ADRENERGIC AGENTS:RECEPTOR DRUG ACTION USESAlpha-1 Norepinephrine Vasoconstrictor Shock, hypotension

Phenylephrine Vasoconstrictor Shosk, hypotension, mydriatic

Beta-1 Dobutamine Cardiac stimulant Inotropic agent (positive,increase heart contractility)

Beta-2 Albuterol Bronchodilator Asthma, emphysema

Isoetharine Bronchodilator Bronchospasm, asthma

Terbutaline Bronchodilator, uterine relaxant

Emphysema, asthma, premature labor

ADRENERGIC AGENTS:RECEPTORss DRUG ACTION USESAlpha and Beta Ephedrine Bronchodilator,

vasoconstrictorNasal decongestant, hypotension

Epinephrine Vasoconstrictor, bronchodilator, cardiac stimulant, allergic reactions

Anaphylaxis, cardiac arrest

Dopamine Vasopressor Shock, hypotension

ADRENERGIC AGENTS:

ADVERSE EFFECTS:• Palpitations, tachycardia, skin flushing,

dizziness, tremors -> mild, do not discontinue• Orthostatic hypotension -> monitor BP, change

positions slowly, advise to sit or lie• Dysrhythmias, chest pain, severe hypotension,

hypertension, chest pain -> DC

ADRENERGIC BLOCKING AGENTSNONSELECTIVE SELECTIVEEqual affinity to beta-1, beta-2

Beta-1 only

Inhibits both beta-1 and beta-2

Inhibits beta-1 receptors of the heart

Inhibits vasoconstriction and bronchodilation

Inhibits vasoconstriction

Causes vasodilation and bronchoconstriction

Causes vasodilation

Cannot be given to patients with HPN with asthma

Can be given to patients with HPN with asthma

ADRENERGIC BLOCKING AGENTSUSES:

a. Alpha-blockers (Alpha1)• drugs with specific affinity for alpha receptors sites• Indicated to patients with diseases associated with

vasoconstrictions (HPN, BPH)• To promote vasodilations

ADRENERGIC BLOCKING AGENTSb. Beta-blockers • cardiovascular problems: hypertension, post-MI,

angina, dysrhythmias, hyperthyroidism*Nonselective beta blockers must be used with

caution in patients with respiratory conditions

**beta blockers should be used with caution in patients with diabetes and hypoglycemia

ADRENERGIC BLOCKING AGENTSINDICATIONS:• - primarily used to treat cardiac-related conditions• -contraindicated with asthma • - Raynaud’s disease, hypertension,

pheochromocytoma, angina, arrhythmias, mitral valve prolapse, glaucoma

ADVERSE EFFECTS:• Diabetes/hypoglycemia: monitor for s/sy (may be

masked by beta-adrenergic blockers) • Bradycardia, heart failure: monitor s/sy• Bronchospasm: withhold medication

CHOLINERGIC AGENTS• parasympathomimetic agents; effects are similar to

acetylcholine (increase activity of receptor sites)• - some directly acting on the PNS -> cholinergic

agonist• - others inhibit acetylcholinesterase

(antiacetylcholinesterase) ->indirect acting cholinergic agents

CHOLINERGIC AGENTSGeneric Brand Uses

Ambenonium Mytelase Myasthenia gravis

Edrophonium Tensilon

Neostigmine Prostigmin

Pyridostigmine Mestinon

Bethanecol Urecholine

Pilocarpine Pilocar Miotic agent; glaucoma

CHOLINERGIC AGENTS

PHARMACOKINETICS

CHOLINERGIC AGONISTS

ANTICHOLINESTERASE DRUGS

Absorption Topical, oral, SQ Oral, IM, IV

Distribution Well-distributed Some can pass BBB

Metabolism Cholinesterase/liverExcretion Urine

ANTICHOLINERGIC AGENTS

• cholinergic blocking agents/parasympatholytic agents

• block the action of acetycholine• parasympathetic response is reduced/blocked• not all cholinergic receptors are blocked, just the

muscarinic receptor sites• may have dual effect (low drug levels stimulate,

high drug levels depress)• effects would bring about SNS effects


USES:• GI and GUT disorders (relax muscles and decrease

GI secretions), and ophthalmic disorders (mydriatics -> refractive errors), bradycardia, Parkinson’s (low dopamine levels -> intensify the stimulating effects of acetylcholine), PRE-OP med (secretions and bradycardia), prevention of vagal nerve stimulation (endoscopy)

Atropine(belladonna alkaloids)

Atropine sulfate Presurgery: reduce bronchial secretions and salivations, minimize bradycardia, treatment of GI spasms


PHARMACOKINETICS:

ABSORPTION Eyes, GIT, mucous membranes, skin;IV –fast

DISTRIBUTION Widely; passes the BBBMETABOLISM Slight CHON-bound; liverEXCRETION Urine

ANTICHOLINERGIC AGENTSADVERSE EFFECTS:• Blurred vision – caution the patient; safety• Constipation/dryness of mucosa – candy/ice

chips/chewing gum; stool softeners; adequate food and fluid intake

• Urinary retention – assess distention• Glaucoma – screen for close-angle glaucoma (open-angle

-> safe); monitor IOP• Confusion/depression/nightmares/hallucinations –

alertness, orientation, mental status• Ortostatic hypotension (infrequent, mild) – monitor BP;

teach patient to position slowly and safely• Palpitations/dysrhythmias – report

PAIN MEDICATIONS1. OPIATE AGONISTS• ACTIONS:• Relieves pain without the loss of consciousness• Act by stimulating opiate receptors in CNS• Controlled substances• May cause primary CNS effects (analgesia, sedation,

respiratory depression, euphoria, mental clouding, etc) and cardiovascular, GIT, GUT effects

• *may produce drug tolerance, dependence and addiction, withdrawal syndrome (restlessness, perspiration, gooseflesh, lacrimation, runny nose and mydriasis)

PAIN MEDICATIONSUSES:• Relieve acute or chronic pain moderate to severe

pain• Preoperative sedation and supplement anesthesia• Reduce anxiety, control edema

PAIN MEDICATIONSCOMMON OPIATE AGONISTS

THERAPEUTIC OUTCOME:• Primary: relief of pain intensity and duration

DRUG BRAND DURATION

Codeine Codeine sulfate/phosphate

4-6 hours

Morphine Morphine sulfate 4-5 hours

Meperidine Demerol 2-4 hours

Tramadol Ultram 4-6 hours

PAIN MEDICATIONSADVERSE EFFECTS

ADVERSE EFFECTS ACTIONS

Lightheadedness, dizziness, sedation, sweating

Supine position, safety, comfort measures, reassurance

Confusion, disorientation

Safety, mental assessment, orientation

Orthostatic hypotension

Monitor BP, positions,

Nausea, vomiting Supine positionConstipation Fluids, stool softeners/laxatives, fiber dietRespiratory depression Monitor respiration

Urinary retention/spasms

Assess distention, report, have patient void

Excessive use/abuse Evaluate response, taper dose for DC, milder analgesic

PAIN MEDICATIONSDRUG INTERACTIONS:

CNS depressants Enhances the depressant effects

Phenytoin Reduces meperidine effect

Carbamazepine Reducing analgesic effect

Warfarin Anticoagulant effect

PAIN MEDICATIONS2. OPIATE PARTIAL AGONISTS• - pharmacologic activity depends on previous

administration of opiate agonist and extent of physical dependence

• - can cause withdrawal syndrome to a patient who is addicted to opiate agonists

USES:• Short-term relief of moderate to severe pain

(cancer, burns, preoperative, obstetric, surgical) THERAPEUTIC OUTCOME:• relief of pain intensity and duration

PAIN MEDICATIONSADVERSE EFFECTS

DRUG INTERACTIONS:

Clamminess, dizziness, sedation, sweating

Supine, safety, assurance, comfort

Nausea, vomiting, dry mouth SameConstipation Continued use, hydration, stool-softeners,

laxatives, roughage dietConfusion, disorientation, hallucinations,

Mental status, orientation, safety

Respiratory depression Respiratory statusExcessive use/abuse Evaluate response, taper dose for DC, milder

analgesic

CNS depressants Enhances depressionsOpiate agonists May have withdrawal symptoms

PAIN MEDICATIONS3. OPIATE ANTAGONISTSA. NALOXONE (NARCAN)• reversal of CNS depressant effects of opiate agonists, opiate

partial agonists and propoxyphene• may precipitate withdrawal syndrome on patients who

have taken opiatesUSES:• DOC: respiratory depressionADVERSE EFFECTS:

Nausea, vomiting Caused by reversal of analgesia; should be used with caution

Mental depression, apathy Mental assessment, orientation

PAIN MEDICATIONS3. OPIATE ANTAGONISTSB. NALTREXONE (REVIA)USES:• Block pharmacologic effects of exogenously administered

opiates• May diminish or eliminate opiate-seeking behaviors • Prevents conditioned abstinence (craving) after withdrawal • Adjunct treatment of alcoholism

THERAPEUTIC OUTCOME:• Improved adherence with substance abuse program because

of reduced craving of opioids• Improved adherence with an alcohol treatment program by

diminishing craving

PAIN MEDICATIONSADVERSE EFFECTS:

DRUG INTERACTIONS:

Nausea, vomiting, anorexia Mild, tend to resolve with therapy; do not discontinue

Headache Mild, tend to resolve with therapy; do not discontinue

Hepatotoxicity Report signs of hepatotoxicity and abnormal liver function tests

Opiate-containing products No benefit; should be avoided during therapy

Clonidine Reduce withdrawal symptoms

PAIN MEDICATIONSNursing considerations : 1. Monitor respiratory depression & hypotension in clients

taking narcotic analgesic. 2. Injury and accident precautions in clients taking narcotic

analgesic. 3. Warn clients about possibility of dependency, and do not

discontinue narcotics abruptly in the narcotic-dependent clients.

4. Naloxone is antidote for narcotic overdose.

ANTIMIGRAINE AGENTS• Migraine headaches – several different syndromes, all of

which include severe, throbbing, pulsating headaches on one side of the head

• Believed to be caused by arterial dilation• Can affect GI and CNS systems (mood and personality

changes)• Two types:

Common migraines Classic migrainesWithout aura With auraSevere, unilateral pulsatingFrequently accompanied by nausea, vomiting, sensitivity to light or sound

ANTIMIGRAINE AGENTS1. ERGOT DERIVATIVES• - cause constriction of cranial blood vessels and decrease

the pulsation of cranial arteries• - reduce the hyperperfusion of the basilar artery vascular

bed

COMMON DRUGS:

dihydroergotamine Migranal IM, IV, nasal spray Rapid treatment of acute attacks

ergotamine Generic Sublingual Prevention and abortion of migraine attacks

ANTIMIGRAINE AGENTSTHERAPEUTIC ACTION:• Block alpha-adrenergic and serotonin receptor sites in the

brain -> constriction of cranial nerves -> decrease in cranial artery pulsation -> decrease in the hyperperfusion of the basilar artery bed

USES:• Prevention and abortion of migraine and vascular

headaches

ANTIMIGRAINE AGENTSPHARMACOKINETICS:

• CONTRAINDICATIONS:• Allergy; CAD/HPN/peripheral vascular disease; liver

impairment• Ergotism (vomiting, diarrhea, seizures) • Pruritus and malnutrition

ABSORPTION Many routes; rapidly absorbed (15-30 mins)

DISTRIBUTION Cannot be used during pregnancyMETABOLISM LiverEXCRETION Bile/stool

ANTIMIGRAINE AGENTSADVERSE EFFECTS:• Numbness, tingling, muscle pains• Pulselessness, weakness, chest pain, arrhythmias, edema,

itching, MI • Nausea, vomiting, diarrhea• Ergotism (n/v, severe thirst, hypoperfusion, angina, BP

changes, confusion, dependency, withdrawal syndrome)

DRUG INTERACTIONS:• Beta blockers – risk of peripheral ischemia and gangrene is

increased

ANTIMIGRAINE AGENTS2. TRIPTANS

DRUG BRAND INDICATIONSsumatriptan Imitrex Acute migraines,

cluster headachesNaratriptan Amerge Acute migrainesRizatriptan Maxaltzolmitriptan ZomigAlmotriptan Axertfrovatriptan FrovaEletriptan Relpax

ANTIMIGRAINE AGENTSTHERAPEUTIC ACTION:• Bind to selective serotonin receptor sites to cause

vasoconstriction of cranial vessels, relieving the signs and symptoms of migraine headache

USES:• Treatment of acute migraine

• PHARMACOKINETICS:ABSORPTION Many sitesDISTRIBUTION Crosses placenta and breast milkMETABOLISM LiverEXCRETION Urine

ANTIMIGRAINE AGENTSCONTRAINDICATIONS AND CAUTIONS:• Allergy; pregnancy; CAD; lactating women; elderly; patients

with renal or hepatic dysfunction ADVERSE EFFECTS:• Numbness, tingling, burning,• Weakness, dizziness, myalgia, vertigo• Dysphagia, abdominal discomforts• BP alterations, chest pains

ANTIMIGRAINE AGENTSNURSING CONSIDERATIONS:

Avoid prolonged use/excessive dosage

To prevent severe adverse effects

Prepare anti-emetics Appropriate drugs to relieve nausea and vomiting

Provide comfort and safety measures

Prevention of headache and to provide pain relief

Assess extremities carefully To ensure that no decubitus ulcers or gangrene are present

Administer for acute headaches Not for prevention

Arrange for safety precautions To prevent patient injury

Monitor BP of any patient with CAD and DC for sign of angina/HPN

To prevent severe vascular effects

ANTIEPILEPTIC AGENTS

EPILEPSY – most prevalent of the neurological disorders• Not single disease but a collection of different syndromes• Sudden discharge of excessive electrical energy from nerve

cells locate within the brain -> seizures• Motor nerve stimulation -> convulsions, toni-clonic muscle

spasm -> injury, tics, spasms


CLASSIFICATION OF SEIZURESA. GENERALIZED SEIZURES

TONIC-CLONIC SEIZURES Grand-mal seizures; tonic-clonic muscle contractions, loss of consciousness, recovery period (confusion and exhaustion)

ABSENCE SEIZURES Petit mal seizures; involve abrupt, brief periods of loss of consciousness; common on children, disappears on puberty

MYOCLONIC SEIZURES Short, sporadic periods of muscle contractions for several minutes; rare

FEBRILE SEIZURES Related to very high fevers with convulsions; children; self-limiting and do not re-appear

STATUS EPILEPTICUS Most dangerous; rapidly recur again and again


CLASSIFICATION OF SEIZURESB. PARTIAL SEIZURES

SIMPLE PARTIAL

Single area; single muscle movement or sensory alteration

COMPLEX PARTIAL

Complex sensory changes (hallucinations, mental distortion, personality changes, loss of consciousness, loss of social inhibitionMotor changes: involuntary urination, chewing motion, diarrhea, etc.


DRUGS FOR TONIC-CLONIC (GRAND MAL SEIZURES)A. HYDANTIONS- stabilize nerve membranes and limit the spread of

excitability, possibly by: promoting the exit of sodium ions from the cell -> returning the cell to a resting membrane potential

- drugs included: phenytoin (Dilantin), ethotoin (Peganone), fosphenytoin (Cerebyx), mephenytoin (Mesantoin)

ACTION: unknown

ANTIEPILEPTIC AGENTS: HYDANTIONS

THERAPEUTIC OUTCOMES: reduced frequency of seizures and reduced injury from seizures

PHENYTOIN (Dilantin)• Treatment of tonic-clonic seizures and status epilepticus• Prevention and treatment of seizures after neurosurgery• A – oral/parenteral; D – GIT; M – liver; E – urine• Adverse effects: nystagmus, ataxia, dysarthria, slurred

speech, tremor, headache• USES: generalized tonic-clonic seizures and partial seizures

ANTIEPILEPTIC AGENTS: HYDANTIONS

ADVERSE EFFECTS:

Nausea, vomiting, indigestion Administer food/milk; increase dosage

Sedation, drowsiness, dizziness, fatigue, lethargy

Dosage adjustment; do not DC; safety

Confusion Mental alertness, orientation; report alterations

Blurred vision Safety

Gingival hyperplasia Personal hygiene

Hyperglycemia Monitor blood glucose, OHA/insulin readjustment

Blood dyscrasias Lab exams; monitor sore throat, fever, purpura, jaundice, weakness

Hepatotoxic Assess for signs; liver functions

ANTIEPILEPTIC AGENTS: BENZODIAZEPINESB. BENZODIAZEPINES• potentiate the effects of GABA that stabilizes nerve cell

membranes• cause muscle relaxation and relieve anxiety• clonazepam (Klonopin), clorazepate (Tranxene), diazepam

(Valium), lorazepam (Atizan)

ACTION: not fully understood; it is thought to enhance GABA

ANTIEPILEPTIC AGENTS: BENZODIAZEPINES• DIAZEPAM (Valium)• Anxiety disorders, acute alcohol withdrawal, tetanus,

convulsive seizures, status epilepticus• Potentiates GABA• A – oral/IM/IV/rectal; M – liver; E – urine

• PHARMACOKINETICS:

ABSORPTION Oral, IM, IV, rectalDISTRIBUTION Widely distributedMETABOLISM LiverEXCRETION Urine

ANTIEPILEPTIC AGENTS: BENZODIAZEPINES• USES: tonic-clonic seizures, status epilepticus, myoclonic

seizures, prevention of seizures after surgery, adjunctive therapy for other seizure disorders or sedation and muscle relaxation

• THERAPEUTIC OUTCOMES: reduced frequency of seizures and reduced injury from seizures

• ADVERSE EFFECTS: SAME =)

ANTIEPILEPTIC AGENTS: BARBITURATES• inhibit impulse conduction in the reticular activating system

(RAS), depress cerebral cortex, alter cerebellar function, depress motor nerve output -> can cause sedation, hypnosis, anesthesia and deep coma

• phenobarbital (Solfoton, Luminal), primidone (Mysoline), mephobarbital (Mebaral)

PHENOBARBITAL (Solfoton, Luminal)• Long-term treatment of tonic-clonic and focal seizures;

emergency control of acute convulsive episodes (status epilepticus, tetanus, eclampsia, meningitis), toni-clonic/focal seizures, sedative, preanesthetic, short-term treatment of insomnia

ANTIEPILEPTIC AGENTS: BARBITURATES• ACTION : general CNS depressant; inhibit impulse

conduction in the reticular activating system (RAS), depress cerebral cortex, alter cerebellar function, depress motor nerve output

• Elevate seizures threshold and prevents spread of electrical

• PHARMACOKINETICS:ABSORPTION Oral, IM, Sub-Q, IV

DISTRIBUTION Widely-distributed

METABOLISM Liver

EXCRETION Urine

ANTIEPILEPTIC AGENTS: BARBITURATESADVERSE EFFECTS:

somnolence, insomnia, vertigo, vertigo, nightmares, anxiety, hallucinations, bradycardia, hypotension, syncope, respiratory depression, withdrawal syndrome

COMMON CONTRAINDICATIONS:• Allergy; pregnancy; lactation; impaired renal or liver

function

ANTIEPILEPTIC AGENTS:NURSING CONSIDERATIONS:• Discontinue drug at any sign of hypersensitivity reaction,

liver dysfunction, severe skin rash – limit reaction and prevent potentially serious reactions.

• Administer with food to alleviate GI upset.• Monitor for adverse effects and treat accordingly.• Provide thorough patient teachings.

ANTIEPILEPTIC AGENTS: DRUGS FOR TREATING ABSENCE (PETIT) SEIZURES

SUCCINIMIDES• Most frequently used • Ethosuximide (Zarontin), Methsuximide (Celontin) • THERAPEUTIC ACTION: unknown; though it suppress the

abnormal electrical activity in the brain • USES: absence seizures

ANTIEPILEPTIC AGENTS: DRUGS FOR TREATING ABSENCE (PETIT) SEIZURES

PHARMACOKINETICS:

CONTRAINDICATIONS:• Allergy, pregnancy and lactation, renal and hepatic

dysfunction, porphyria • ADVERSE EFFECTS: same =)

ABSORPTION GITDISTRIBUTION Can pass through placenta and breastmilkMETABOLISM LiverEXCRETION Urine

ANTIEPILEPTIC AGENTS: DRUGS FOR TREATING PARTIAL SEIZURESA. CARBAMAZEPINE (Tegretol)ACTIONS: blocks the reuptake of norepinephrine and decreases the

release of norepinephrine and the rate of dopamine and GABA turnover

USES: partial seizures and tonic-clonic; not effective on absence seizures;

trigeminal neuralgia; bipolar disorder THEARAPEUTIC OUTCOME: SAME ADVERSE EFFECTS: SAME +• Orthostatic hypotension, hypertension- monitor BP, etc• Dyspnea, edema – s/sy; intervene• Nephrotoxicity – monitor lab, UO, • Hepatotoxic – anorexia, n/v, jaundice, hepatomegaly, splenomegaly,

abnormal liver functions

ANTIEPILEPTIC AGENTS: DRUGS FOR TREATING PARTIAL SEIZURESB. GABAPENTIN (Neurontin)

• ACTION: unknown • USES: used in combination with other anticonvulsants;

postherpetic neuralgia

DRUGS USED FOR PARKINSON’S DISEASEPARKINSON’S DISEASE• Incidence is higher in men than women; all races and ethnic

groups are affected• Motor tremors (resting), muscle rigidity (inflexibility), akinesia

(loss of muscle movement), disturbances of posture and balance (motor)

• Orthostatic hypotension, nocturnal sleep disturbances with daytime somnolence, depression, dementia, inability to make decisions (nonmotor)

• Manifestations are caused by deterioration of dopaminergic receptors causing depletion of dopamine causing neurologic deficits

• There should be balance between dopamine (inhibitory) and acetylcholine (excitatory)

• Imbalance causes parkinsonism manifestations

DRUGS USED FOR PARKINSON’S DISEASETwo types:

GOAL OF TREATMENT: minimizing the symptoms

PRIMARY/ IDIOPATHIC PARKINSONISM SECONDARY PARKINSONISM

Reduction in dopamine-producing cells Head trauma, intracranial infections, tumors, drug exposure

DRUGS USED FOR PARKINSON’S DISEASE: DOPAMINERGIC DRUGS• Drugs that increase the effects of dopamine• Dopamine itself does not cross the BBB; dopamine-like and

increased dopamine concentration indirectly ->increase dopamine levels in the brain

• Amantadine, apomorphine, bromocriptine, levodopa, carbidopa, pergolide, pramipexole, ropinirole

• ACTIONS: increasing the levels of dopamine in the

substantia nigra or directly stimulating the dopamine receptors

• USES: relief of signs and symptoms of idiopathic Parkinson’s

disease

DRUGS USED FOR PARKINSON’S DISEASE: DOPAMINERGIC DRUGSCOMMON DRUGS FOR PARKINSON’S DISEASE:

Levodopa Dopar Mainstay; precursor; crosses BBB-> replacement therapy; used in combination w/ carpidopa (inhibits dopa decarboxylase) , levodopa can be decreased in dosage->reducing adverse effects

Amantadine Symmetrel Antiviral; increase the release of dopamine

Apomorphine Apokyn Newest adjunctive therapy; directly bind with receptors ; “hypomobility” episodes during the wearing off

Carbidopa Sinemet Enzyme inhibitor; reduces metabolism of levodopa

DRUGS USED FOR PARKINSON’S DISEASE: DOPAMINERGIC DRUGSPHARMACOKINETICS:

ADVERSE EFFECTS:• CNS effects: anxiety, nervousness, headache, malaise,

fatigue, confusion, mental changes, blurred vision, muscle twitcing, ataxia

• Peripheral effects: anorexia, nausea, vomiting, dysphagia and constipation or diarrhea, arrhythmias, hypotension, urinary retention

ABSORPTION Well-absorbed from the GITDISTRIBUTION Crosses placenta, breastmilkMETABOLISM LiverEXCRETION Urine

DRUGS USED FOR PARKINSON’S DISEASE: ANTICHOLINERIGCSACTIONS: blocks the action of Ach to help normalize Ach-

dopamine imbalance• Reduce the degree of rigidity, tremors, and drooling

COMMON DRUGS:

benztropine Cogentin Oral/IM/IV; parkinsonism and Parkinson-like symptoms (phenotiazines)

biperiden Akineton Oral/IM; adjunct therapydiphenhydramine Bendryl Adjunct; elderly patients

DRUGS USED FOR PARKINSON’S DISEASE: ANTICHOLINERIGCSPHARAMACOKINETICS:

ADVERSE EFFECTS:• CNS effects: disorientation, confusion, memory loss,

agitation, nervousness, delirium, dizziness, light-headedness, weakness

• PNS: dry mouth, nausea, vomiting, constipation, tachycardia, palpitations, hypotension, urinary retention

ABSORPTION GIDISTRIBUTION Placenta, breastmilkMETABOLISM LiverEXCRETION

DRUGS USED FOR PARKINSON’S DISEASE: ANTICHOLINERIGCSCONTRAINDICATIONS:• Allergy, glaucoma (narrow-angled), MG, CAUTION:• Tachycardia, hypertension/hypotension (because of SNS

effect), pregnancy and lactation, liver dysfunction NURSING CONSIDERATIONS:• Give medication with meals• Monitor bowel function (constipation)• Let patient void before taking the drug• Patient safety

GENERAL AND LOCAL ANESTHETICSGENERAL ANESTHETICS• Analgesia, unconsciousness, amnesia; block reflexes,

Balanced Anesthesia• >Preop meds – anticholinergics: decrease secretions and

prevents bradycardia• >Sedative-hypnotics: relax the patient, amnesia, decrease

parasympathetic response• >Antiemetics: decrease nausea and vomiting• >Antihistamines: decrease allergic reactions• >Narcotics:analgesia

GENERAL AND LOCAL ANESTHETICSStages while on anesthesia:

• INDUCTION- beginning to stage3; danger is stage 2 (systemic stimulation)

• MAINTENANCE- stage 3 until surgical procedure is complete• RECOVERY- discontinuation of anesthetic until patient

regained consciousness, movement and communication (life support system must be available)

STAGE1 Analgesia stage

Loss of pain sensation; patient still conscious and able to communicate

STAGE2 Excitement stage

Signs of sympathetic stimulation

STAGE3 Surgical anesthesia

Relaxation of skeletal muscles, regular respirations; loss of eye reflexes; operation can be performed

STAGE4 Paralysis Very deep CNS depression, death can occur

GENERAL ANESTHESIABARBITURATES• IV drugs used to induce rapid anesthesia, then maintained

with inhaled drug

• NONBARBITURATE

thiopental Pentothal Most widely used IV anesthetics, rapid onset of action, ultrashort recovery period; no analgesic effect

methohexital

Brevital Rapid onset; short recovery period; no analgesic effect; must not come in contact with silicone; respiratory depression and apnea-> available intubation

midazolam Generic Prototype; causes nausea and vomiting, potent amnesiac

GENERAL ANESTHESIAANESTHETIC GASES

USES: sedation, hypnosis, anesthesia, amnesia and unconsciousness to allow painful surgeries

Nitrous oxide Blue cylinder Very potent analgesic, can cause hpoxia (administer w/ O2); weakest

Cyclopropane Orange cylinder Rapid onset and action; not good analgesic; pain, headache, nausea, vomiting, delirium during recovery

Ethylene Red cylinder Less toxic

GENERAL ANESTHESIAPHARMACOKINETICS:

ADVERSE EFFECTS: CV and respiratory depression manifestations, nausea and vomiting, somnolence, delirium,

CONTRAINDICATIONS:• Status asthmaticus CAUTIONS:• CVD, hypotension, shock

ABSORPTION Lipid solubleDISTRIBUTION Distributed widelyMETABOLISM LiverEXCRETION

GENERAL ANESTHESIA• LOCAL ANESTHETICSMODES OF ADMINISTRATION:1. TOPICAL- cream, lotion, ointment, drop; mucous

membranes; systemic effect is rare2. INFILTRATION – injecting directly into the tissues3. FIELD BLOCK – injecting the anesthetic all around the area

to be operated; more intense (comes in contact with all of the nerve endings surrounding the area)

4. NERVE BLOCK – injecting the nerve (peripheral: sensory and motor aspects; central: roots of the nerves of the spinal cord; epidural: space where the nerves emerge; caudal block; sacral area)

GENERAL ANESTHESIAACTION: cause temporary interruption in the production and

conduction of nerve impulses• Affects the permeability of nerve membranes to sodium

ions-> prevents sodium ions from entering-> prevents depolarization-> nerve cannot be stimulated

ADVERSE EFFECTS:• Associated with route of administration and amount that is

absorbed systemically• CV and respiratory depression

nervous system

Documents

central nervous system

nervous system2 physiology

nerve activity

presynaptic nerve

motor nerves neuron

efferent nerves

reactionblock receptor

peripheral receptors