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Semis - Nervous System

The document provides a comprehensive overview of the nervous system, detailing its divisions, the role of neurons, and the physiological mechanisms of action potentials and neurotransmitters. It discusses the autonomic nervous system, including its two divisions (sympathetic and parasympathetic), and the effects of various drugs on these systems, including adrenergic and cholinergic agents. Additionally, it covers pain medications, specifically opiate agonists and partial agonists, their uses, adverse effects, and drug interactions.
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0% found this document useful (0 votes)
194 views16 pages

Semis - Nervous System

The document provides a comprehensive overview of the nervous system, detailing its divisions, the role of neurons, and the physiological mechanisms of action potentials and neurotransmitters. It discusses the autonomic nervous system, including its two divisions (sympathetic and parasympathetic), and the effects of various drugs on these systems, including adrenergic and cholinergic agents. Additionally, it covers pain medications, specifically opiate agonists and partial agonists, their uses, adverse effects, and drug interactions.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

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
- neuron: structural unit of the nervous system

 PHYSIOLOGY OF THE NERVOUS SYSTEM


- Electrical impulses and chemical messengers – transmit information throughout the body

NEURONS
Parts 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)

 Afferent fibers – axons that run from peripheral receptors to CNS


 Efferent fibers – CNS to periphery to stimulate muscles or glands

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

NEUROTRANSMITTER
- Chemical
- Stimulates postsynaptic cells either by exciting or inhibiting them
- Once released from the synaptic cleft, it reacts with very specific receptor sites to cause reaction

Selected neurotransmitters:

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 Brain; inhibits nerve activity; prevents overexcitability or
(GABA) 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
 The afferent and efferent nerves are known collectively as PERIPHERAL NERVOUS SYSTEM
 The efferent system is divided into motor nervous system (skeletal muscle) and autonomic nervous system

DRUGS AFFECTING THE AUTONOMIC NERVOUS SYSTEM

- Automatic and self-governing


- Involuntary or visceral nervous system -> little conscious awareness
- Hypothalamus, medulla, spinal cord
- Integrates parts of the CNS and PNS to automatically react to changes
- Regulates BP, HR, respiration, temp, water balance, urinary excretion and digestive functions

 TWO DIVISIONS:
SYMPATHETIC PARASYMPATHETIC
Major neurotransmitter Catecholamines: Acetylcholine (Ach)
-epinephrine, norepinephrine,
dopamine
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; Decrease v/s, increase GI;
vasoconstriction vasodilation
Constipation Diarrhea
Urinary retention Urinary incontinence
Myadriasis Miosis
Bronchodilation Bronchoconstriction
Relaxation of muscles Excitation of muscles
Dry eyes Lacrimation
Dry mouth Salivation

 FOUR GROUPS OF ANS MEDS


DRUGS DESCRIPTION
Cholinergic agents - medications that cause effects in the body
similar to those produced by acetylcholine
- Parasympathomimetic agents
- Mimic the action of parasympathetic division
Adrenergic 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

1. ADRENERGIC AGENTS
- sympathomimetic drugs
- mimic the effects of SNS
- adrenergic nervous system may be stimulated by two broad classes of drugs:

Classification by chemical
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

Classification by 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:
1. Alpha (α)
alpha-1 receptors vasoconstriction of blood vessels
alpha-2 receptors mediator of negative feedback; preventing release of norepinephrine

2. Beta (β)
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)

3. Dopaminergic
- improves symptoms associated with Parkinson’s disease
- dopamine -> increases urine output (stimulates specific receptors in the kidneys)

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 USES


Alpha-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, Emphysema, asthma,
uterine relaxant premature labor
Alpha and Beta Ephedrine Bronchodilator, Nasal decongestant,
vasoconstrictor hypotension
Epinephrine Vasoconstrictor, Anaphylaxis, cardiac
bronchodilator, arrest
cardiac stimulant,
allergic reactions
Dopamine Vasopressor Shock, hypotension

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

2. ADRENERGIC BLOCKING AGENTS


- plugs the alpha or beta receptors -> prevents other agents from stimulating the receptors
- sympatholytic drugs which lyse/block the effects of the SNS
- beta blockers (antiHPN; “-olol”)

TYPES OF BETA BLOCKERS


NONSELECTIVE SELECTIVE
Equal 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

USES:
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
b. 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 cause bronchoconstriction
*beta blockers should be used with caution in patients with diabetes and hypoglycemia
->mask s/sy of hypoglycemia; induce hypoglycemic effects of insulin

*Therapeutic action and adverse effects associated with these drugs are related to their ability to react with specific
adrenergic receptor sites without activating them

INDICATIONS:
- 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

DRUG INTERACTIONS:
Antihypertensive agents, beta-adrenergic agents, NSAIDS

3. CHOLINERGIC AGENTS
- parasympathomimetic agents; effects are similar to acetylcholine (increase activity of receptor sites)
- mimics action of PNS
- some directly acting on the PNS -> cholinergic agonist
- others inhibit acetylcholinesterase (antiacetylcholinesterase) ->indirect acting cholinergic agents

Generic Brand Uses


Ambenonium Mytelase Myasthenia gravis
Edrophonium Tensilon
Neostigmine Prostigmin
Pyridostigmine Mestinon
Bethanecol Urecholine
Pilocarpine Pilocar Miotic agent; glaucoma

>myasthenia gravis – descending paralysis; decreased number of Ach receptor; presence of enzyme
>guillane barre – ascending paralysis

PHARMACOKINETICS
CHOLINERGIC AGONISTS ANTICHOLINESTERASE DRUGS
Absorption Topical, oral, SQ Oral, IM, IV
Distribution Well-distributed Some can pass BBB
Metabolism Cholinesterase/liver
Excretion Urine

ADVERSE EFFECTS:
- Nausea, vomiting, diarrhea, abdominal cramping: dose-related
- Dizziness, hypotension: monitor BP; change positions slowly; sit, lie
- Bronchospasm, wheezing, bradycardia: withhold, re-evaluate patient

DRUG INTERACTIONS:
Atropine and antihistamines: antagonists

4. 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 Atropine sulfate Presurgery: reduce bronchial secretions


(belladonna alkaloids) and salivations, minimize bradycardia,
treatment of GI spasms

PHARMACOKINETICS:
ABSORPTION Eyes, GIT, mucous membranes, skin;IV –fast
DISTRIBUTION Widely; passes the BBB
METABOLISM Slight CHON-bound; liver
EXCRETION Urine

ADVERSE 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

DRUG INTERACTIONS:
Amantadine, antidepressants – may potentiate anti cholinergic effects -> confusions and hallucinations

PAIN MEDICATIONS

1. OPIATE AGONISTS
- derived from opium (morphine, heroin)
-formerly narcotics (induce stupor or sleep/sedative/addictive effect -> needs S2 license)

ACTIONS:
- Relieves pain without the loss of consciousness
- Act by stimulating opiate receptors in CNS
- Controlled substances (may cause dependence)
- 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)

USES:
- Relieve acute or chronic pain moderate to severe pain
- Preoperative sedation and supplement anesthesia
- Reduce anxiety, control edema

COMMON OPIATE AGONISTS


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

THERAPEUTIC OUTCOME:
Primary: relief of pain intensity and duration

COMMON ADVERSE 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 position
Constipation Fluids, stool softeners/laxatives, fiber diet
Respiratory depression Monitor respiration
Urinary retention/spasms Assess distention, report, have patient void
Excessive use/abuse Evaluate response, taper dose for DC, milder analgesic

DRUG INTERACTIONS:
CNS depressants Enhances the depressant effects
Phenytoin Reduces meperidine effect
Carbamazepine Reducing analgesic effect
Warfarin Anticoagulant effect

2. OPIATE PARTIAL AGONISTS


- pharmacologic activity depends on previous administration of opiate agonist and extent of physical dependence
- similar potency to morphine as analgesic
- it may also cause tolerance after prolonged use
- increasing dosage, increases adverse effect
- 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

DRUG BRAND NAME DURATION


Nalbuphine Nubain 3-6

ADVERSE EFFECTS
Clamminess, dizziness, sedation, sweating Supine, safety, assurance, comfort
Nausea, vomiting, dry mouth Same
Constipation Continued use, hydration, stool-softeners, laxatives,
roughage diet
Confusion, disorientation, hallucinations, Mental status, orientation, safety
Respiratory depression Respiratory status
Excessive use/abuse Evaluate response, taper dose for DC, milder analgesic

DRUG INTERACTIONS:
CNS depressants Enhances depressions
Opiate agonists May have withdrawal symptoms

3. OPIATE ANTAGONISTS
A.NALOXONE (NARCAN)
- reversal of CNS depressant effects of opiate agonists, opiate partial agonists and propoxyphene
- there is no pharmacologic effect on patients who have not taken opiates
- may precipitate withdrawal syndrome on patients who have taken opiates

USES:
- DOC: respiratory depression

ADVERSE EFFECTS:
Nausea, vomiting Caused by reversal of analgesia; should be used with caution
Mental depression, apathy Mental assessment, orientation

B. NALTREXONE (REVIA)
- active after oral administration; longer duration

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

ADVERSE EFFECTS:
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

DRUG INTERACTIONS:

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


Clonidine Reduce withdrawal symptoms

Nursing 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 migraines
Without aura With aura
Severe, unilateral pulsating
Frequently accompanied by nausea, vomiting, sensitivity to light or sound

1. 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

THERAPEUTIC 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

PHARMACOKINETICS:
ABSORPTION Many routes; rapidly absorbed (15-30 mins)
DISTRIBUTION Cannot be used during pregnancy
METABOLISM Liver
EXCRETION Bile/stool

CONTRAINDICATIONS:
- Allergy; CAD/HPN/peripheral vascular disease (could be exacerbated); liver impairment (may affect metabolism
and excretion
- Ergotism (vomiting, diarrhea, seizures)
- Pruritus and malnutrition

ADVERSE EFFECTS:
- Related to drug-induced vascular constriction
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 -> should be avoided

2. TRIPTANS
- new class of drugs that cause cranial vascular constriction and relief of migraine headache pain
- not associated with the CV and GI effects of ergot derivatives
- choice of triptan depends on the personal experience and existing medical condition

TRIPTANS
DRUG BRAND INDICATIONS
sumatriptan Imitrex Acute migraines, cluster headaches
Naratriptan Amerge Acute migraines
Rizatriptan Maxalt
zolmitriptan Zomig
Almotriptan Axert
frovatriptan Frova
Eletriptan Relpax

THERAPEUTIC 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 (not used as prevention)

PHARMACOKINETICS:
ABSORPTION Many sites
DISTRIBUTION Crosses placenta and breast milk
METABOLISM Liver
EXCRETION Urine

CONTRAINDICATIONS 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

DRUG INTERACTIONS:
Ergot drugs – risk of prolonged vasoactive reactions
MAOI – severe adverse effects

NURSING 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 To prevent severe vascular effects
DC for sign of angina/HPN

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
- Antiepileptics -> depends on the type of epilepsy and patient tolerance to adverse effects

CLASSIFICATION OF SEIZURES
- Correct diagnosis -> correct medication -> prevent future seizures -> fewest problems/adverse

A. GENERALIZED SEIZURES
- begin in one area of the brain and spreads rapidly on both hemispheres -> loss of consciousness
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

B. PARTIAL SEIZURES
- focal seizures; one area of the brain and do not spread to the entire organ; depends on where excessive electrical
discharge is happening

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 inhibition
Motor 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
- less sedating from others
- drugs included: phenytoin (Dilantin), ethotoin (Peganone), fosphenytoin (Cerebyx), mephenytoin (Mesantoin)

ACTION: unknown

 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

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

ADVERSE EFFECTS:
Nausea, vomiting, indigestion Administer food/milk; increase dosage
Sedation, drowsiness, dizziness, Dosage adjustment; do not DC; safety
fatigue, lethargy
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

B. 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


 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, rectal
DISTRIBUTION Widely distributed
METABOLISM Liver
EXCRETION Urine

- Bradycardia and tachycardia, urinary retention, incontinence, drug dependency

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 =)

C. BARBITURATES AND BARBITURATE-LIKE DRUGS


- 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

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

ADVERSE 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

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.

DRUGS FOR TREATING ABSENCE (PETIT) SEIZURES


- Involve a brief, sudden and self-limited loss of consciousness; patient may just stare into space or blink rapidly
(people may be unaware of the 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

PHARMACOKINETICS:
ABSORPTION GIT
DISTRIBUTION Can pass through placenta and breastmilk
METABOLISM Liver
EXCRETION Urine

CONTRAINDICATIONS:
- Allergy, pregnancy and lactation, renal and hepatic dysfunction, porphyria

ADVERSE EFFECTS: same =)

DRUGS FOR TREATING PARTIAL SEIZURES


- Involve only a part of the brain and originates on one site/focus; s/sy depends on what part of the brain is
affected by excessive electrical impulse is occurring

DRUGS:

A. 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

B. GABAPENTIN (Neurontin)

ACTION: unknown

USES: used in combination with other anticonvulsants; postherpetic neuralgia


DRUGS USED FOR PARKINSON’S DISEASE

PARKINSON’S DISEASE – chronic progressive disorder of CNS


- 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
- Two types:
PRIMARY/ IDIOPATHIC PARKINSONISM SECONDARY PARKINSONISM
Reduction in dopamine-producing cells Head trauma, intracranial infections, tumors, drug
exposure
- Symptoms start insidiously (weakness and tremors then progressively involve movement disorders throughout
the body
- Symptoms usually begin on one side then become bilateral ; upper part of the body is affected first
- Dementia - slowing thought process, lapses, loss of impulse control
- History taking, PA, positive response to dopaminergic treatment

GOAL OF TREATMENT: minimizing the symptoms because there is no cure

DOPAMINERGIC DRUGS
- Drugs that increase the effects of dopamine -> more effective than anticholinergics
- Dopamine itself does not cross the BBB; dopamine-like and increased dopamine concentration indirectly
->increase dopamine levels in the brain -> effective for as long as neurons are intact
- Amantadine, apomorphine, bromocriptine, levodopa, carbidopa, pergolide, pramipexole, ropinirole

ACTIONS: increasing the levels of dopamine in the substantia nigra or directly stimulating the dopamine receptors ->
restore the balance between the inhibitory and stimulating neurons

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

COMMON 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

PHARMACOKINETICS:
ABSORPTION Well-absorbed from the GIT
DISTRIBUTION Crosses placenta, breastmilk
METABOLISM Liver
EXCRETION Urine

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

ANTICHOLINERIGCS
- Parkinson’s disease is brought about by imbalance between decreased dopamine and increased acethylcoline,
so the need for anticholinergics

ACTIONS: 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 therapy
diphenhydramine Bendryl Adjunct; elderly patients

PHARAMACOKINETICS
ABSORPTION GI
DISTRIBUTION Placenta, breastmilk
METABOLISM Liver
EXCRETION

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

CONTRAINDICATIONS:
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 ANESTHETICS

- Drugs that are used to complete or partial loss of sensation

GENERAL ANESTHETICS
- Analgesia, unconsciousness, amnesia; block reflexes,

Balanced Anesthesia
- Use of combination of drugs, each with specific effect-> analgesia, muscle relaxation, unconsciousness, amnesia
rather than use of single drug. The following agents are:
>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

Stages while on anesthesia:


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

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)

TYPES OF GENERAL ANESTHESIA:

BARBITURATES
- IV drugs used to induce rapid anesthesia, then maintained with inhaled drug

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

NONBARBITURATE

midazolam Generic Prototype; causes nausea and vomiting, potent amnesiac

ANESTHETIC GASES
- Passes the bronchi, alveoli, capillary system, heart, systemic
- High lipid affinity (CNS)

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

THERAPEUTIC ACTIONS:

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

PHARMACOKINETICS:
ABSORPTION Lipid soluble
DISTRIBUTION Distributed widely
METABOLISM Liver
EXCRETION

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

CONTRAINDICATIONS:
Status asthmaticus

CAUTIONS:
CVD, hypotension, shock

LOCAL ANESTHETICS
- Limited areas of the body
- Loss of temperature, touch, proprioception, skeletal muscle tone (recovery in reverse)
- Should not be absorbed systemically -> CV and CNS depression
- benzocaine, procaine, tetracaine, pramoxine, lidocaine

MODES OF ADMINISTRATION:
1. TOPICAL- cream, lotion, ointment, drop; mucous membranes; systemic effect is rare
2. INFILTRATION – injecting directly into the tissues
3. 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)

ACTION: 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

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