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136 Cards in this Set

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What are the PNS Trasmitters?
-Acetylcholine
-Norepinephrine
-Epinephrine
A.N.E
How many Transmitters do CNS have?
more than 24
What are the characteristics of the Blood-Brain Barrier?
-impedes the entry of drugs into the brain
-provides protection
-however, blocks therapeutic drug agents as well.
PAIN CONTROL

What are ANALGESIC?
-Loss of sensibility to PAIN

ex: Aspirin, Tylenol and Morphine
Aspirin, Tylenol and Morphine
PAIN CONTROL

What are ANESTHESIA?
-Loss of pain and all other sensation as well.
Lidocaine and nitrous oxide
LOCAL ANESTHEICS

MOA of LIDOCAINE?
-Stops Neuro conduction inthe axon by blocking sodium channel
-Non-selective action
What is the ROUTE for LIDOCAINE?
-Topically for Surface Anesthesia
-Injection such as nerve blocks, epidural and spinal analgesics
When is LIDOCAINE use?
-Pain Control such as for procedures like suturing
-Also used to treat for DYSRHYTHMIAS
What are the ADVERSE EFFECTS for LIDOCAINE?
-They only occur with excessively high doses and resulting systemic absorption

*CNS: excitation followed by depression
*cardiac suppresion-bradycardia, heart block
*Allergic reactions are rare
*In utero-depressed contractility and prolonged labor
C.C.A.In
General Anesthetics?
Are drugs that produce unconsciousness and lack of responsiveness to ALL painful Stimuli
Types of General Anesthetics?
Inhaled and Intravenous
Inhaled Anesthetics?
Halothane and Nitrous Oxide
Intravenous Anesthetics?
-Thiopental (Pentothal)
-Ketamine->dissolove anesthesia
Medications Used for Anesthesia *Before*?
pre-Anesthetic medication

*atropine, valium
Medications used for Anesthesia *during*?
Neuromuscular Blocking Agents

*Succinylcholine*

**NEUROSMUSCULAR BLOCKING AGENTS PREVENT CONTRACTION OF ALL SKELETAL MUSCLES, INCLUDING THE DIAPHRAGM AND OTHER MUSCLE CONTRATION, THAT IS WHY DURING SURGERY PT'S NEED MECHANICAL SUPPORT FOR RESPIRATION
Medications used for AnesthesiA *AFTER*?
POST-ANESTHETIC AGENTS

* ANTIRMITICS, ANALGESIC
WHAT ARE ANALGESICS?
MEDICATIONS THAT RELIEVE PAIN WITHOUT CAUSING LOSS OF CONSCIOUSNESS!

"PAINKILLERS"
WHAT IS PAIN FOR PATIENTS?
PAIN IS A SUBJECTIVE AND INDIVIDUAL EXPERIENCE. IT CAN BE DEFINED AS WHATEVER THE PERSON SAYS IT IS AND IT EXIST WHENEVER HE OR SHE SAYS IT DOES.
WHAT IS PAIN THRESHOLD?
LEVEL OF STIMULUS NEEDED TO PRODUCE THE PERCEPTION OF PAIN.
WHAT IS PAIN TOLERANCE?
THE AMOUNT OF PAIN A PERSON CAN ENDURE WITHOUT HINDERING NORMAL FUNCTION
WHAT IS THE PATHOPHYSIOLOGY OF PAIN?
THE NEURAL MECHANISMS BY WHICH PAIN IS PERCEIVED ARE PART OF A PREOCESS THAT INVOLVES 4 MAJOR STEPS:

1.TRANSDUCTION
2.TRANSMISSION
3.PERCEPTION
4.MODULATION
What 2 Types of pain are there?
NOCICEPTIVE PAIN AND NEUROPATHIC PAIN
What is NOCICEPTIVE PAIN?
pain resulting from an activation of primary afferent nociceptors by MECHANCIAL, THERMAL or CHEMICAL stimuli.
What is NEUROPATHIC PAIN?
Pain resulting from damage to Peripheral Nervous System or Central Nervous system tissue or from altered processing of pain in the central nervous system.
What is an OPIOD ANALGESIC?
MORPHINE
What is an OPIOID ANTAGONISTS?
NALOXONE (NARCAN)
WHAT are NON-OPIOID Anagesics?
-Ibuprofen (Motrin, Advil)
-Acteaminophen (Tylenol)
What is an OPIOID?
An opioid is a chemical substance that has a morphine-like action in the body. The main use is for pain relief.

These agents work by binding to opioid receptors, which are found principally in the central nervous system and the gastrointestinal tract.

The receptors in these two organ systems mediate both the beneficial effects, and the undesirable side effects. There are four broad classes of opioids:

*endogenous opioid peptides (opioids produced naturally in the body);
*opium alkaloids, such as morphine (the first alkaloid isolated from opium) and codeine;

*semi-synthetic opioids, such as heroin and oxycodone; and
fully synthetic opioids, such as pethidine and methadone.

*Although the term opiate is often used as a synonym for opioid, it is more properly limited to the natural opium alkaloids and the semi-synthetics derived from them.
What is an OPIATE?
In medicine, the term opiate describes any of the narcotic alkaloids found in opium.
What is NARCOTIC?
A narcotic is an addictive drug, derived from opium, that reduces pain, induces sleep and may alter mood or behavior.

The derivation of the word is from the Greek word narkotikos, meaning "benumbing or deadening," and originally referred to a variety of substances that induce sleep (such state is narcosis).
Topic= OPIOIDS

what is the MOA of MORPHINE?
MOA : act to mimic OPIOID like neurotransmitters and bind to opioid receptors
Topic= OPIOIDS

What are the IND of MORPHINE?
Morphine is used to
-relief of moderate to severe pain
-sedation
-cough suppression
WHAT ARE MORPHINE'S PHARMACOLOGICAL EFFECTS?
-ANALGSIA
-SEDATION
-EUPHORIA
-DECREASED ANXIETY
-RESPIRATORY DEPRESSION
-COUGH SUPPRESSION
-CONSTIPATION
-URINARY RETENTION
-ORTHOSTATIC HYPTENSION
WHAT ARE MORPHINE'S ABSORPTION AND DISTRIBUTIONS?
*Routes-Oral, IM, IV, or SubQ,
epidural, intrathecal
-only a small amount crosses the blood brain barrier
-oral morphine has strong first pass effect
What are morphine's adverse effects?
AE:
*Respiratory effects
*Constipation
*Orthostatic Hypotension
*Urinary Retention
*Cough Suppression
*Emesis
*Euphoria/ Dysphoria
*Can Cause tolerance and dependence
What are MORPHINE's CAUTIONS/ CI?
-Pregnancy/ L&D - depression of newborn
-head injury
-infants
-elderly
what are MORPHINE'S DRUG INTERACTIONS?
-CNS DEPRESSANTS
-ANTI-CHOLINERGICS
-ANTI-HYPERTENSIVES
WHAT ARE MORPHINE'S TOXCITY?
-COMA
-REPIRATORY DEPRESSION
-PINPOINT PUPILS
NURSING IMPLICATIONS?
-PAIN ASSESSMENT
-ADVERSE EFFECTS
-PATIENT TEACHING
ADDICTION to OPIOIDS?
-opioid tolerance
-opioid dependence
-psychological dependence

"pain is what the patient says it is"
NARCOTIC WITHDRAWAL ABSTINENCE SYNDROME?
-BEGINS 10 HRS AFTER LAST DOSE
-DURATION 7-10DAYS
*SYMPTOMS
-SWEATING, YAWNING, RHINNOREA
-ANOREXIA, TREMOR, IRRITABILITY
-WEAKNESS, NAUSEA, VOMITING, DIARRHEA, ABDOMINAL CRAMPS, BONE AND MUSCLE PAIN
-
OPIOID ANTAGONIST

***NALOXONE/ (NARCAN)***

MOA??
MOA: COMPETES AT OPIOID RECEPTOR SITES TO BLOCK OPIOID ACTIONS.
WHAT IS THE PHARMACOKINETICS OF NALOXONE (NARCAN)?
-IV =immediate effects and last an hour
-half life is about 2 hrs
WHAT DRUG IS A NON-CENTRALLY ACTING ANALGESICS?
-CLONIDINE
Pain management in special populations?
children
*assessment challenges
*tools
*physical indicatiors of pain
*neonates and infants have high sensitivity to medication dude to underdevolped liver

Elderly
*undertreament of pain
*heightened drug sensitivity
MEDS for PD to Inc Dopamine are Dominergic Meds

they are LEVADOPA-CARBIDOPA (Sinemet) -> this is a combo drug.

What's the MOA?
MOA:

*LEVOPADA: promotes syntheis of dopamine. Transported across BBB and then converted to dopamine in CNS.

*CARBIDOPA: Enhances effects of LEVADOPA, blocks peripheral conversion of levadopa to dopamine. (No therapeutic effects). (For it can be more available in the CNS).
When is LEVOPADA-Carbidopa(Sinemet) used?
This med is used for PARKINSON's Disease.
*it doesn't cure PD, but prolongs the quality of life.
*it takes awhile for the med to be therapeutic and it wears off over time.
What are the ADVERSE EFFECTS of LEVOPADA-Carbidopa?
1.Nausea/vomiting
2.dyskinesias: involuntary mov'ts.
3.postural hypotension
4.psychosis (Halluncination and Paranoia)
What are the Drug interactions for LEVOPADA-Carbidopa?
1. Monamine oxidase inhibitors
(Psychotic meds for depression)
2. antipsychotic drugs (blocks the dopamine -> dec the effects)
3.anti-cholinergics (INC the effects of LEVOPADA)
What are the nursing considerations when a patient is taking LEVOPADA-Carbidopa?
1. high protein meals -can affect the absorbtion of LEVO and it can DEC the absorption.
2.On-off phenomena-sometimes the effects of the drugs wears off and PD is INC
3.Drug holiday-person stops taking the drug for a short period of time (10days) to see if it's still effective.
PD MED

What is the MOA of PRAMIPEXOLE (Mirapex)?
MOA: activates DOPAMINE receptors in BASAL GANGLIA
When do you use MIRAPEX?
Mirapex is used for PD alone in early disease, with levadopa in advanced disease
What are the adverse effects of MIRAPEX?
Similiar to LEVODOPA, but less dyskinesias( invol. movement)
ALZHEIMER'S DISEASE MEDS

What is the MOA of DONEPEZIL/ ARICEPT?
DONEPEZIL/ ARICEPT are cholinesterase inhibitors.

MOA: acts as cholinesterase inhibitors-prevents breakdown of acetycholine by acetylcholinesterase. Results in INC ACETEYLCHOLINE and enhanced cholinergic effects.
When are DONEPEZIL/ ARICEPT used?
these meds are used in the early stages of AD and they are not effective in the later stages.
What are the Adverse effects of DONEPEZIL/ ARICEPT?
1.GI symptoms
2.dizziness
3.bronchoconstriction

**Similar to Cholinergic effects**
What are the Drug Interactions with DONEPEZIL/ ARICEPT?
-Antihistamines
-tricyclic antidepressants (block the cholinergic receptor, which will reduce the effects of the med)
ALZHEIMER'S DISEASE MEDS

*NMDA receptor antagonists*
DRUG:MEMANTINE

what is the MOA of MEMANTINE?
MOA:
Blocks specific NMDA receptor sites. NMDA receptors regulate CA entry into neurons.

**INC CA impairs learning and memory, neurodegenration .
**MEMANTINE blocks -> DEC CA entry
**Basically, too much CA causes memory loss**
When is MEMANTINE use?
IND: Memantine is used for MODERATE to SEVERE Alzheimer's Disease.
AD MED
What are the Adverse Effects of MEMANTINE?
AE:
-Minimal Head Aches
-Dizziness
-Confusion
-constipation
What are the Drug Interaction for MEMANTINE?
DI:

SODIUM BICARBONATE: any drug that cause URINE to be ALKALINE will DEC the excretion of MEMANTINE = INC in the body = TOXIC to the body!

MEMANTINE is excreted better normal URINE
MULTIPLE SCLEROSIS MEDS

IMMUNOMODULATORS ->INTERFERON beta-1a/Avonex(IM)or Rebif(Sq)

What's its MOA?
MOA:
Suppresses autoimmune destruction of myelin.
**it suppresses it by stoppin the body from attacking the its own myelin**
**It delays the progression of MS, it doesn't cure it!!**
When is IMMUNOMODULATORS ->INTERFERON beta-1a/Avonex(IM)or Rebif(Sq)used?
IND:
this med is used for MS
What are the adverse Effects of IMMUNOMODULATORS ->INTERFERON beta-1a/Avonex(IM)or Rebif(Sq)used?
-Flu-like symptoms= short term over time, they'll get use to meds.
-hepatotoxicity=injure the liver cells
-bone marrow suppression=
dec= prod rbc -> ANEMIC
-dec wbc-> infection
-dec platelets-> inc Bleeding
MEDS for MULTIPLE SCLEROSIS

IMMUNOSUPPRESSANTS

MED=MITOXANTRONE/NOVANTRONE what it's MOA?
MOA:
Suppresses the production of immune system cells ->dec AUTO-IMMUNE destruction of MYELIN
When do you use IMMUNOSUPPRESSANTS

MED=MITOXANTRONE/NOVANTRONE?
IND:

This med is used for MS pts who do not respond to other drugs. this is given IV and every 3 months!
What are the Adverse Effects of IMMUNOSUPPRESSANTS

MED=MITOXANTRONE/NOVANTRONE?
AE:
-Bone Marrow Suppression=very toxic to the bone marrow
-Cardiotoxicity=Irreversible damage to the heart
-Fetal harm

Nursing Consideration: Infection Protection bc the DEc of Prod of WBC!!
EPILEPSY/ SEIZURES

DEF??
Epilepsy: group of seizure disorders characterized by excessive excitability of the neurons in CNS. You don't need to have an EPILEPSY to ahve a SEIZURE-healthy people can have this w/ many reasons and don't know why.
What are the two type of SEIZURES?
1. PARTIAL SEIZURES:
BEGIN LOCALLY
A.Simple partial Seizures: one hemishphere. NO LOSS OF CONSCIOUSNESs
B. Complex Partial Seizures: Both Hemispheres, Change in LOC

GENERALIZED SEIZURES
-Both Hemispheres, Loss of CONSCIOUSNESS

A.Absence (Petit mal): brief LOC but no motor activity (blank stare)
B.Tonic-Clonic:stiffening of body, followed by jerking of extremities, LOC
ANTI-EPILEPTIC DRUGS:
Traditional AED =PHEYTOIN/ Dilantin what its MOA?
MOA: NA channel blocker-> slows the entry of Na into neurons -> suppresses neuron activity. Selective for hyperactive neurons & preventsthe spread of other areas. Doesn't affect the healthy neurons..only the bad ones.
When is Traditional AED =PHEYTOIN/ *Dilantin* med use?
IND:
-partial seizures, tonic-clonic seizures
(Serum levels: narrow therapeutic range 10-20mcg/ml)
**Important to monitor drug levels**
What are the adverse effets of Traditional AED =PHEYTOIN/ *Dilantin*?
AE (At therapeutic levels)
*mild sedation
*gingival hyperplasia=growth of gum tissue
*skin rash*
*teratogenic=harmful to the fetus

AT TOXIC LEVELS:
**ATAXIA=unsteady gait
**INC sedation
**Cognitive impairment
**double Vision
**Nystagmus(back and forth Mov't of eyes) the pupil goes goes back N forth.
What are the DRUG INTERACTIONS of Traditional AED =PHEYTOIN/ *Dilantin*?
DI: P450 Hepatic drug metabolizing enzyme inducer: it DEC the effects of other drugs like WARFARIN, Oral Contraceptives, glucocorticoids.

Drugs that INC DILANTIN levels by reducing it's metabolism, which may inc TOXICITY
*Alcohol
*Cimetidine (anti-ulcer med)
*Valium
*Valproic Acid
What are the nursing consideration for this MED
Traditional AED =PHEYTOIN/ *Dilantin*?
-monitor drug levels
-take at night it cause sedation
-don't abruptly stop med= it'll cause seizures (slowly gradually dec it bc it might create REBOUND SEIZURES)
AED MED TRADITIONAL

Carbamazepine/ *Tegretol*(similar to Dilantin) whats the MOA
MOA:Sodim channel blocker, same mechanism as DILANTIN
What are the nursing consideration for this MED
Traditional AED =PHEYTOIN/ *Dilantin*?
-monitor drug levels
-take at night if cause sedation
-don't abruptly stop med= it'll cause seizures (slowly gradually dec it bc it might create REBOUND SEIZURES)
When is this MED used?

AED MED TRADITIONAL
Carbamazepine/ *Tegretol*
IND: this med is used for partial seizures
*tonic clonic seizures
*bipolar disorders
*trigeminal
*or glossopharynegeal nerve pain
What are the Adverse effects of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
AE:
*minimal CNS cognitive effects
*visual disturbance=nystagmus, blurred vision
*Bone Marrow suppression (some patients)
*Ataxia: affect gait
*Rash
AED MED TRADITIONAL

Carbamazepine/ *Tegretol*(similar to Dilantin) whats the MOA
MOA:Sodim channel blocker, same mechanism as DILANTIN
What are the Drug Interaction of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
*P450 enzyme inducer (same as dilantin)
*Dilatin causes dec in Tegretol levels
*grapefruit juce (inhibits the metobolism of Tegretol which will inc the effects)
When is this MED used?

AED MED TRADITIONAL
Carbamazepine/ *Tegretol*
IND: this med is used for partial seizures
*tonic clonic seizures
*bipolar disorders
*trigeminal
*or glossopharynegeal nerve pain
What are the Adverse effects of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
AE:
*minimal CNS cognitive effects
*visual disturbance=nystagmus, blurred vision
*Bone Marrow suppression (some patients)
*Ataxia: affect gait
*Rash
AED MED TRADITIONAL
VALPROIC Acid/ Depakote what the MOA?
Blocks both Na and Ca channels -> suppressed the neuron activity
When do you use AED MED TRADITIONAL
VALPROIC Acid/ Depakote?
IND:
all partial and generalized seizures, bipolar disorders and migraine
What are the Drug Interaction of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
*P450 enzyme inducer (same as dilantin)
*Dilatin causes dec in Tegretol levels
*grapefruit juce (inhibits the metobolism of Tegretol which will inc the effects)
What are the adverse effects of TRADITIONAL
VALPROIC Acid/ Depakote?
AE:

*GI
*nausea
*vomitting
*indigestion
*hepatotoxicity=toxic to the liver
*pancreatitis
*teratogenic=harmful to the fetus
AED MED TRADITIONAL
VALPROIC Acid/ Depakote what the MOA?
Blocks both Na and Ca channels -> suppressed the neuron activity
What is the MOA of TRADITIONAL *PHENOBARBITAL*?
MOA: This med will sedate the the patient. it effects GABA-> CNS Sedation. This med is cheapest and oldest med for Seizures
What are the nursing consideration for this MED
Traditional AED =PHEYTOIN/ *Dilantin*?
-monitor drug levels
-take at night if cause sedation
-don't abruptly stop med= it'll cause seizures (slowly gradually dec it bc it might create REBOUND SEIZURES)
When do you use AED MED TRADITIONAL
VALPROIC Acid/ Depakote?
IND:
all partial and generalized seizures, bipolar disorders and migraine
When DO YOU USE TRADITIONAL *PHENOBARBITAL*?
*PARTIAL SEIZURES
*TONIC-CLONIC SEIZURES
(SOMETIMES USED AS A SLEEPING AID)
What are the adverse effects of TRADITIONAL
VALPROIC Acid/ Depakote?
AE:

*GI
*nausea
*vomitting
*indigestion
*hepatotoxicity=toxic to the liver
*pancreatitis
*teratogenic=harmful to the fetus
What are the ADVERSE EFFECTS of PHENOBARBITAL?
*Sedation
*Interferes with Metabolism of Vitamin D (need for Ca absorbtion and Vit K is needed for clotting).

*Respiratory depression at toxic levels (Respiratory arrest)

*Dependent bc its a barbiturate
AED MED TRADITIONAL

Carbamazepine/ *Tegretol*(similar to Dilantin) whats the MOA
MOA:Sodim channel blocker, same mechanism as DILANTIN
MEDS for MUSCLE SPASMS and SPATICITY
(Centrally-Acting Meds)
**Diazepam/ Valium** MOA?
MOA:
Acts to enhance GABA -> CNS Sedation
What is the MOA of TRADITIONAL *PHENOBARBITAL*?
MOA: This med will sedate the the patient. it effects GABA-> CNS Sedation. This med is cheapest and oldest med for Seizures
When is this MED used?

AED MED TRADITIONAL
Carbamazepine/ *Tegretol*
IND: this med is used for partial seizures
*tonic clonic seizures
*bipolar disorders
*trigeminal
*or glossopharynegeal nerve pain
When do you use
**Diazepam/ Valium** ?
IND:

*relieve muscle spasms and spaticity
*Decrease PAIN
*active seizures
*anti-anxiety
What are the Adverse effects of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
AE:
*minimal CNS cognitive effects
*visual disturbance=nystagmus, blurred vision
*Bone Marrow suppression (some patients)
*Ataxia: affect gait
*Rash
When DO YOU USE TRADITIONAL *PHENOBARBITAL*?
*PARTIAL SEIZURES
*TONIC-CLONIC SEIZURES
(SOMETIMES USED AS A SLEEPING AID)
What are the ADVERSE EFFECTS of PHENOBARBITAL?
*Sedation
*Interferes with Metabolism of Vitamin D (need for Ca absorbtion and Vit K is needed for clotting).

*Respiratory depression at toxic levels (Respiratory arrest)

*Dependent bc its a barbiturate
What are the Adverse Effects of **Diazepam/ Valium**?
*CNS Depression
*Physical dependence
What are the Drug Interaction of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
*P450 enzyme inducer (same as dilantin)
*Dilatin causes dec in Tegretol levels
*grapefruit juce (inhibits the metobolism of Tegretol which will inc the effects)
MEDS for MUSCLE SPASMS and SPATICITY
(Centrally-Acting Meds)
**Diazepam/ Valium** MOA?
MOA:
Acts to enhance GABA -> CNS Sedation
AED MED TRADITIONAL
VALPROIC Acid/ Depakote what the MOA?
Blocks both Na and Ca channels -> suppressed the neuron activity
MEDS fOR MUSCLE SPASMS and SPATICITY
(centrally-Acting MEDS)

**BACLOFEN/Lioresal**
MOA:

Suppress hyperactive reflexes, mimics actions of GABA on the Spinal Cord
When do you use
**Diazepam/ Valium** ?
IND:

*relieve muscle spasms and spaticity
*Decrease PAIN
*active seizures
*anti-anxiety
When do you use AED MED TRADITIONAL
VALPROIC Acid/ Depakote?
IND:
all partial and generalized seizures, bipolar disorders and migraine
What are the adverse effects of TRADITIONAL
VALPROIC Acid/ Depakote?
AE:

*GI
*nausea
*vomitting
*indigestion
*hepatotoxicity=toxic to the liver
*pancreatitis
*teratogenic=harmful to the fetus
What is the MOA of TRADITIONAL *PHENOBARBITAL*?
MOA: This med will sedate the the patient. it effects GABA-> CNS Sedation. This med is cheapest and oldest med for Seizures
What are the Adverse Effects of **Diazepam/ Valium**?
*CNS Depression
*Physical dependence
When DO YOU USE TRADITIONAL *PHENOBARBITAL*?
*PARTIAL SEIZURES
*TONIC-CLONIC SEIZURES
(SOMETIMES USED AS A SLEEPING AID)
What are the nursing consideration for this MED
Traditional AED =PHEYTOIN/ *Dilantin*?
-monitor drug levels
-take at night if cause sedation
-don't abruptly stop med= it'll cause seizures (slowly gradually dec it bc it might create REBOUND SEIZURES)
MEDS fOR MUSCLE SPASMS and SPATICITY
(centrally-Acting MEDS)

**BACLOFEN/Lioresal**
MOA:

Suppress hyperactive reflexes, mimics actions of GABA on the Spinal Cord
AED MED TRADITIONAL

Carbamazepine/ *Tegretol*(similar to Dilantin) whats the MOA
MOA:Sodim channel blocker, same mechanism as DILANTIN
What are the ADVERSE EFFECTS of PHENOBARBITAL?
*Sedation
*Interferes with Metabolism of Vitamin D (need for Ca absorbtion and Vit K is needed for clotting).

*Respiratory depression at toxic levels (Respiratory arrest)

*Dependent bc its a barbiturate
When is this MED used?

AED MED TRADITIONAL
Carbamazepine/ *Tegretol*
IND: this med is used for partial seizures
*tonic clonic seizures
*bipolar disorders
*trigeminal
*or glossopharynegeal nerve pain
MEDS for MUSCLE SPASMS and SPATICITY
(Centrally-Acting Meds)
**Diazepam/ Valium** MOA?
MOA:
Acts to enhance GABA -> CNS Sedation
When do you use
**Diazepam/ Valium** ?
IND:

*relieve muscle spasms and spaticity
*Decrease PAIN
*active seizures
*anti-anxiety
What are the Adverse Effects of **Diazepam/ Valium**?
*CNS Depression
*Physical dependence
What are the Adverse effects of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
AE:
*minimal CNS cognitive effects
*visual disturbance=nystagmus, blurred vision
*Bone Marrow suppression (some patients)
*Ataxia: affect gait
*Rash
MEDS fOR MUSCLE SPASMS and SPATICITY
(centrally-Acting MEDS)

**BACLOFEN/Lioresal**
MOA:

Suppress hyperactive reflexes, mimics actions of GABA on the Spinal Cord
What are the Drug Interaction of AED MED TRADITIONAL
Carbamazepine/ *Tegretol*?
*P450 enzyme inducer (same as dilantin)
*Dilatin causes dec in Tegretol levels
*grapefruit juce (inhibits the metobolism of Tegretol which will inc the effects)
AED MED TRADITIONAL
VALPROIC Acid/ Depakote what the MOA?
Blocks both Na and Ca channels -> suppressed the neuron activity
When do you use AED MED TRADITIONAL
VALPROIC Acid/ Depakote?
IND:
all partial and generalized seizures, bipolar disorders and migraine
What are the adverse effects of TRADITIONAL
VALPROIC Acid/ Depakote?
AE:

*GI
*nausea
*vomitting
*indigestion
*hepatotoxicity=toxic to the liver
*pancreatitis
*teratogenic=harmful to the fetus
What is the MOA of TRADITIONAL *PHENOBARBITAL*?
MOA: This med will sedate the the patient. it effects GABA-> CNS Sedation. This med is cheapest and oldest med for Seizures
When DO YOU USE TRADITIONAL *PHENOBARBITAL*?
*PARTIAL SEIZURES
*TONIC-CLONIC SEIZURES
(SOMETIMES USED AS A SLEEPING AID)
What are the ADVERSE EFFECTS of PHENOBARBITAL?
*Sedation
*Interferes with Metabolism of Vitamin D (need for Ca absorbtion and Vit K is needed for clotting).

*Respiratory depression at toxic levels (Respiratory arrest)

*Dependent bc its a barbiturate
MEDS for MUSCLE SPASMS and SPATICITY
(Centrally-Acting Meds)
**Diazepam/ Valium** MOA?
MOA:
Acts to enhance GABA -> CNS Sedation
When do you use
**Diazepam/ Valium** ?
IND:

*relieve muscle spasms and spaticity
*Decrease PAIN
*active seizures
*anti-anxiety
What are the Adverse Effects of **Diazepam/ Valium**?
*CNS Depression
*Physical dependence
MEDS fOR MUSCLE SPASMS and SPATICITY
(centrally-Acting MEDS)

**BACLOFEN/Lioresal**
MOA:

Suppress hyperactive reflexes, mimics actions of GABA on the Spinal Cord
When do you use BACLOFEN/ Lioresal?
IND:

Reduce Spasticity in PTS with Cerebral Palsy, Spinal Cord injury and MS.
What are the Adverse Effects of BACLOFEN/ Lioresal?
AE:

*CNS Depression
*NAUSEA
*CONSTIPATION
*URINARY RETENTION
What are the nursing consideration when a patient is on BACLOFEN/ Lioresal?
*gradual Withdrawal. Not to stop it abruptly bc the PT may have REBOUND SPASMS

Given PO or an IMPLANT pump and its set at a set dose to teh spinal cord.