Pharmacology Flashcards
Pharmacokinetics vs Pharmacodynamics
Pharmacokinetics: What the BODY does TO a drug once it enters the system. Involves absorption, distribution, metabolism, & excretion.
Pharmacodynamics: what the DRUG does TO the body
Absorption
Drug absorbed from site of administration. Faster absorption from IV vs from oral
Distribution: The ___ system sends drug throughout the body. Drugs attach to [large/small] ____ which are produced by the [organ] then are released to travel as an unbound drug to get into certain tissues (e.g. to cross the ___).
The CIRCULATORY system sends drug throughout the body. Drugs attach to LARGE PLASMA PROTEINS which are produced by the LIVER then are released to travel as an unbound drug to get into certain tissues (e.g. to cross the BLOOD BRAIN BARRIER).
In an individual with liver disease, may have FEWER plasma proteins = LESS ABLE TO RETAIN a drug in the circulatory system -> drug may get to tissues FASTER; might need to adjust dosing
Impact of exercise on pharmacokinetics?
Consider absorption, distribution, metabolism, & excretion with the example of injecting insulin into an exercising muscle
Exercise -> Increased tissue HEAT -> increased DIFFUSION across the membranes and into the bloodstream (post insulin injection -> rapid transfer of drug into bloodstream -> could result in hypoglycemia)
Blood is also shunted TOWARD exercising muscle and AWAY from liver & kidneys, which can impact those organs’ roles/efficacy in drug metabolism & excretion
Metabolism: occurs primarily in the [organ]. ____ convert drug from an active -> less active or inactive form.
Impact of aging or disease states on metabolism?
Metabolism: occurs primarily in the LIVER. ENZYMES convert drug from an active -> less active or inactive form.
Older adults may have decreased liver function (due to aging or liver disease). If drug isn’t being metabolized in the liver, it will continue to circulate & exert its effect! May need to adjust dosage.
Excretion: occurs in the [organ]. Water-soluble drugs excreted in ___. Fat soluble drugs are ___ to be further metabolized until more water soluble & able to be excreted by kidneys
May need to adjust dosing for those w/impaired renal function
Excretion: occurs in the KIDNEYS. Water-soluble drugs excreted in URINE. Fat soluble drugs are REABSORBED & RECIRULATED to be further metabolized until more water soluble & able to be excreted by kidneys
May need to adjust dosing for those w/impaired renal function
Therapeutic index is the ratio of ___ over ____.
A wide/large therapeutic index means a drug [is relatively safe / needs to be closely monitored] vs a small therapeutic index means ___.
Therapeutic index = ratio of MEDIAN TOXIC DOSE over MEDIAN EFFECTIVE DOSE.
A wide/large therapeutic index = relatively SAFE
Small/narrow therapeutic index = may require more FREQUENT MONITORING of drug levels in blood (e.g. warfarin)
The median effective dose is when ____.
The median toxic dose is when ___.
Median effective dose = 50% of the population responds to the drug in a desired manner (desired effect)
Median toxic dose = dose at which 50% of population would exhibit toxic effects (not desired)
Acetylcholine
- Involved with the [parsympathetic / sympathetic / both parsympathetic and sympathetic) nervous system(s)
- Activated by _____
- Plays a role in ____
- Involved with ___ (dz)
- Involved with BOTH the parsympathetic AND sympathetic nervous system
- Activated by acetylcholinesterase
- Role in COGNITION & MEMORY
- Involved with ALZHEIMER’S DZ
Dopamine
Important in regulating motor control in the [brain structure].
Important in mood and emotions in [brain structure]
Dopamine:
- Monoamine
- Important in regulating motor control in BASAL GANGLIA
- Important in mood and emotions in HYPOTHALAMUS
Excess dopamine can be involved with ___ (dz)
Too little dopamine is typical in ____ (dz)
Excess dopamine can be involved w/PSYCHOSIS
Too little dopamine is typical in PARKINSON’S DZ
Norepinephrine
- Role in ____ nervous system
- Action ends in reuptake from ___ & storage in ____
Involved with ___ (dz)
Norepinephrine
- Role in AUTONOMIC nervous system
- Action ends in reuptake from SYNAPTIC CLEFT & storage in NEURON
Involved with DEPRESSION
Serotonin
Important w/ ____ & ____ (cog functions)
Involved with ___(dz)
Serotonin
Important w/ MOOD AND BEHAVIOR
Involved with DEPRESSION
Gamma-aminobutyric acid (GABA)
Receptor location?
Involved with ___ (dz)
Gamma-aminobutyric acid (GABA)
Receptors THROUGHOUT CNS
Involved with ANXIETY / SEIZURES / SPASTICITY
Discuss the relationship between dopamine and acetylcholine in Parkinson’s Disease.
In PD, goal is to [increase/decrease] DA, or [increase/decrease] ACh
PD: Progressive degeneration of dopaminergic neurons in BG upsets the balancing effect between DA & ACh in the brain
Address by: INCREASING DA vs DECREASING ACh
Levadopa-carbadopa is the mainstay in the treatment of PD. What’s the purpose of the levadopa? The carbadopa?
Levadopa: is a dopamine precursor, can cross the blood brain barrier, where it is converted to dopamine by the dopa decarboxylase enzyme in brain
Carbadopa: deactivates the dopa decarboxylase enzyme in the blood stream -> allows L-DOPA to move into brain & be beneficial!
At high doses of levadopa, we can see undesirable GI side effects? Why? What can help to prevent that?
Dopa decarboxylase (breaks down L-DOPA -> dopamine) exists both in the blood stream and in the brain. With levadopa alone, you need a large enough dose of L-DOPA to make sure enough gets across the blood brain barrier to be beneficial in the brain. BUT this large dose can -> undesirable GI side effects
Solution: Carbadopa acts to deactivate the dopa decarboxylase enzyme in the blood stream -> allows L-DOPA to move into brain & be beneficial!
Peak sinemet timing is ____ post administration
Peak sinemet timing is 1 HOUR post administration
Sinemet side effects
- Cardiovascular
- GI
- Behavioral
- Neuro
Sinemet Side effects:
- Cardiovascular: arrhythmias, postural hypotension; monitor BP closely
- GI: nausea/vomiting
- Behavioral: anxiety, depression, confusion, hallucinations
Neuro: Dyskinesias: tics, tremors, choreoathetoid movements; onset >=5 years after initiation of dopamine-replacement therapy. Common w/those diagnosed at younger age or those who need higher levels of dopa.
What is the role of dopamine agonists in the treatment of PD?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
DA Agonists
Action: Bind and activate post-synaptic dopamine receptors.
Use: monotherapy in early PD & <65yo, OR combination therapy later in disease to decrease dose of levadopa needed
Benefits: Longer half life, sustained stimulation of dopamine
Examples:
Bromocriptine (Parlodel)
Pramipexole (Mirapex)
Ropinirole (Requip)
Side effects: (similar to Sinemet/L-Dopa)
Cardiovascular: arrhythmias, postural hypotension; monitor BP closely
GI: nausea/vomiting
Behavioral: anxiety, depression, confusion, hallucinations
Dyskinesias: tics, tremors, choreoathetoid movements; onset >=5 years after initiation of dopamine-replacement therapy. Common w/those diagnosed at younger age or those who need higher levels of dopa.
Impulse control disorders (e.g. compulsive buying, gambling, impulsive sexual behaviors)
What is the role of MAOB (monoamine oxidase type B) inhibitors in the treatment of PD?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
MAOB Inhibitors
- Action: inhibits monoamine oxidase type B enzyme, which is responsible for breaking down dopamine in brain = more dopamine available in brain
Benefits: Reduce motor fluctuations & delay need for L-dopa -> ?neuroprotective effect
Examples: Selegiline (Eldepryl, Emsam)
Side effects
GI issues - could exacerbate peptic ulcers
Insomnia
What is the role of COMT (Catechol-O-methyltransferase) inhibitors in the treatment of PD?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
Catechol-O-methyltransferase (enzyme) metabolizes levodopa in the brain; inhibit it -> more dopamine available in brain
- Used as combination therapy with L-dopa
- Examples: Entacapone (Comtan), Tolcapone (Tasmar)
- Side Effects: c/f liver damage - monitor LFTs
Discuss the 5 global approaches to augmenting the effects of DA in PD
- Levadopa-carbadopa [action/site/enzyme involved]
- Dopamine agonists… [action and site]
- [enzyme] breaks down dopamine in the brain (inhibit this via [drug type] -> more DA available in the brain)
- [enzyme] metabolizes levodopa in the brain (inhibit this via [drug type] -> more DA available in brain)
- Anticholinergics [action/site]
- Levadopa-carbadopa: L-dopa crosses blood brain barrier, once in brain the dopa decarboxylase enzyme converts it to dopamine; separately, carbadopa acts to deactivate the dopa decarboxylase enzyme in the blood stream -> allows L-DOPA to move into brain & be beneficial!
- Dopamine agonists bind and activate post-synaptic dopamine receptors
- Monoamine oxidase type B enzyme breaks down dopamine in the brain (inhibit this with MAOB inhibitors -> more DA available in the brain)
- Catechol-O-methyltransferase metabolizes levodopa in the brain (inhibit this via COMT inhibitors -> more DA available in brain; used in combination w/L-DOPA)
- Anticholinergics decrease ACh in brain
What is the role of anticholinergics in the treatment of PD?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
Anticholinergics
- Goal: to decrease ACh levels in brain
- Used as monotherapy in individuals <70yo who may have tremor but no significant bradykinesia or gait dysfunction
- E.g. Trihexyphenidyl;
Benztropine (Cogentin)
- Side Effects: Dry mouth, Dry skin, Tachycardia, Dilated pupils, Slowed GI/GU motility
What is the role of Amantadine (Symetrel) in the treatment of PD?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
Amantadine
- Unclear mechanism of action (drug is also an antiviral; also used to stimulate arousal!)
- Used as monotherapy for early PD OR in combination w/L-dopa with moderate PD (for those who experience “wearing off” effects”)
- Side effects (similar to Sinemet):
Cardiovascular: arrhythmias, postural hypotension; monitor BP closely
GI: nausea/vomiting
Behavioral: anxiety, depression, confusion, hallucinations
Dyskinesias: tics, tremors, choreoathetoid movements; onset >=5 years after initiation of dopamine-replacement therapy. Common w/those diagnosed at younger age or those who need higher levels of dopa.
Alzheimer’s disease
- Involves the progressive destruction of neurons in the __ and ___, leading to cognitive impairment. Specific cognitive symptoms include: ___.
Key categories of pharmacological treatment include ___, ___, and ___.
Alzheimer’s disease:
- Involves the progressive destruction of neurons in the CEREBRAL CORTEX and HIPPOCAMPUS, leading to cognitive impairment.
- Symptoms: Memory loss, loss of language, confusion, restlessness, mood swings, forgetfulness & loss of concentration (often missed early on!)
- Key categories of pharmacological treatment include CHOLINESTERASE INHIBITORS, MEMANTINE, (N-methyl D-aspartate (NMDA) antagonist, aka Namenda) and STATINS (may have a neuroprotective effect).
What is the role of cholinesterase inhibitors in the treatment of Alzheimer’s?
- Mechanism of action?
- Benefits?
- Examples (drug names)?
- Side effects?
Cholinesterase Inhibitors
- Action: Block acetylcholinesterase -> decreased ACh availability (normally, acetylcholinesterase is responsible for making ACh in synaptic cleft -> increases ACh availability)
- Attempts to SLOW neural process, but cannot reverse it
- E.g.: Donepezil (Aricept),
Galantamine (Razadyne), Rivastigmine (Exelon) - can be given via transdermal patch (daily)!
Side effects: Nausea, vomiting, Diarrhea, Weight loss, Mm weakness, Generalized pain, Fatigue, Dizziness, Insomnia
What is the role of Memantine (Namenda) in the treatment of Alzheimer’s?
- Mechanism of action?
- Benefits?
- Side effects?
Memantine (Namenda)
- Action: reduces glutamate levels & thus neuronal injury (it’s an N-methyl D-aspartate (NMDA) antagonist)
- Used to delay cognitive & physical deficits in moderate to severe AD
- Can be used in conjunction with AChesterase inhibitors
- No known side effects
What is the role of statins in the treatment of Alzheimer’s?
- Mechanism of action?
- Benefits?
Statins
- May also have neuroprotective effect through alteration of amyloid regulation process in brain
Anxiety
- Key receptor: ____
- Definition: ____
- Symptoms include…
- Treatment mainstay [drug type]
Anxiety
- Key receptor: GABA
- Defined as…excessive worry & anxiety that is difficult to control. Can cause distress/impairment on more days than not for at least 6 months.
- Symptoms:
somatic/psychological; include restlessness, mm aches/tension, fatigue, GI symptoms
- Treatment: Benzodiazepines
Psychosis
- Key neurotransmitter : ____
- Symptoms…
- Most common type = ___
- Treatment mainstay [drug type]
Psychosis
- Key neurotransmitter: dopamine
- Symptoms: delusions, hallucinations, inappropriate mood, bizarre behaviors
- Most common type = schizophrenia
- Treatment: antipsychotic drugs block DA receptors (ideally w/out sedation); have typical & atypical
Depression
- Key neurotransmitter : an [increase/decrease] in ___ and ___
- Defined as…
- Symptoms…
- Treatment:
- 1st generation antidepressants include…
- 2nd generation antidepressants include…
Depression
- Key neurotransmitter: DECREASE in norepinerphrine & serotinin
- Defined as...symptoms that occur during the same 2-week period that represent a change from normal function, and must include either a depressed mood or a loss of interest/pleasure nearly every day as well as =>5 additional symptoms, e.g.: Weight loss/gain incr/decr appetite Fatigue Loss of energy Feelings of worthlessness Excessive guilt Diminished ability to think/concentrate
- Treatment:
– 1st generation antidepressants: tricyclic antidepressants, MAO inhibitors (concerns for safety & averse effects)
2nd generation: selective serotonin reuptake inhibitors (SSRIs) & selective serotonin-norepinephrine inhibitors (SNRIs) - No differences within a class or across class of antidepressants
Disease modifying agents in ALS
Riluzole for ALS
Disease modifying agents in HD
NONE exist for HD
Disease modifying agents in MS
Disease modifying agents in MS
- Beta interferons (Avonex, Betaseron, Rebif)
- Copaxone
- Gilenya
- Novantrone
- Tysabri
Disease modifying agents in Alzheimer’s Dz
Acetyl-choline-esterase inhibitors (e.g. exelon, aricept)
N-methyl D-aspartate (NMDA) antagonists (e.g. Namenda)
What drug types are associated with falls in the elderly? (4)
Benzodiazepines (anxiety)
Hypnotics
Sedatives
Antidepressants (depression)
Anxiety is typically treated with [drug type]. Most of these drug names end with -___. These act by binding to inhibitory __ receptor sites in the brain leading to some sedation which decreases muscle tension and affects thought processes/behaviors. Typical side effects include… (4). Any complications/changes that need to be made to dosing over time?
Anxiety is typically treated with BENZODIAZEPINES. Most of these drug names end with -EPAM (e.g. Diazepam/Valium, Lorazepam/Ativan). These act by binding to inhibitory GABA receptor sites in the brain leading to some sedation which decreases muscle tension and affects thought processes/behaviors. Typical side effects include SEDATION, DIZZINESS, ATAXIA, and DIFFICULTY W/SPEED AND ACCURACY. May develop a TOLERANCE over time, with related complications of dependence and withdrawal. Associated with increased risk for FALLS in the elderly.
1st generation antipsychotics are [typical / atypical] antipsychotics and have [lots of / fewer] side effects. Examples include… They act by blocking ___ receptors to decrease [ negative / positive ] symptoms, for example ____. Side effects fall into three general camps:
Anticholinergic effects (e.g. [5]; you need to monitor for __ issues!)
Antiadrenergic effects (e.g. __, __, and __)
Histamine blockade effects (e.g. __ and ___).
____ side effects - abnormal movement patterns. early, you may see ___ when they can’t sit still, vs later may see __ ___ which are repetitive involuntary movements of the face/arms/legs/fingers.
1st generation antipsychotics are TYPICAL antipsychotics and have LOTS OF side effects. Examples include: e.g. HALDOL, and others that end in -INE (Thorazine, Fluphenazine, Thioridazine). They act by blocking DOPAMINE receptors to decrease POSITIVE symptoms, for example HALLUCINATIONS, DELUSIONS, and PARANOIA. Side effects fall into three general camps:
Anticholinergic effects (e.g. DRY MOUTH, BLURRED VISION, CONSTIPATION, URINARY RETENTION, TACHYCARDIA. You need to monitor for CARDIAC issues!)
Antiadrenergic effects (e.g. ORTHOSTASIS, DIZZINESS, SEDATION)
Histamine blockade effects (e.g. SEDATION and WEIGHT GAIN).
EXTRAPYRAMIDAL side effects - abnormal movement patterns. early, you may see AKATHESIA when they can’t sit still, vs later may see TARDIVE DYSKINESIA which are repetitive involuntary movements of the face/arms/legs/fingers.
2nd generation antipsychotics are considered [typical / atypical] antipsychotics and have [lots of / fewer] side effects. Examples include… These act to decrease [negative/positive] symptoms, for example ___. Side effects include…, so you need to watch for signs of low __ and __ abnormalities. Of the 2nd generation drugs [drug name] as the fewest side effects.
2nd generation antipsychotics are considered ATYPICAL antipsychotics and have FEWER side effects. Examples include (others that end in -INE, including Clozapine, Olanzapine/Zyprexa, Quetiapine/Seroquel, Risperidone/Risperdal, Abilify). These act to decrease NEGATIVE symptoms, for example inability to experience PLEASURE or LIMITED SPEECH. Side effects include WEIGTH GAIN, HYPERGLYCEMIA, and LIPID ABNORMALITIES, so you need to watch for signs of low BLOOD SUGAR and LIPID abnormalities. Of the 2nd generation drugs ABILIFY has the fewest side effects.
Extrapyramidal side-effects are most commonly associated with ___ drug class, with examples of specific drugs including…. Early on, these abnormal movement patterns may appear as ___ or as [disease]-like symptoms, or acute ___. Later, we may see __ ___ which involves repetitive involuntary movements of the face, arms, legs, fingers, especially in [males/females] and [older/younger] populations.
Extrapyramidal side-effects are most commonly associated with 1ST GENERATION ANTIPSYCHOTICS drug class, e.g. HALDOL, and others that end in -INE (Thorazine, Fluphenazine, Thioridazine). Early on, these abnormal movement patterns may appear as AKATHESIAS (i.e. can’t sit still) or as PARKINSON’S-like symptoms, or acute DYSTONIAS. Later, we may see TARDIVE DYSKINESIA which involves repetitive involuntary movements of the face, arms, legs, fingers, especially in FEMALES and ELDERLY populations.
Drug classes for treating depression include…(3). Describe neurotransmitters involved, examples/drug names, primary side effects, and considerations for each.
Antidepressants:
- Tricyclic antidepressants - inhibit reuptake of NOREPINEPHRINE and SEROTONIN in presynaptic terminal. Lots of NTs involved = LOTS of side effects (ACh, Histamine, and adrenergic receptor-related side effects). Examples: Amitriptyline/Elavil, Desipramine/Norpramin, Imipramine/Tofranil. Needs close monitoring due to NARROW THERAPEUTIC INDEX
- Monomine Oxidase Inhibitors (MAOIs): inhibit MAO A and MAO B enzymes to prevent breakdown of NE, DA, and Serotonin in brain! Side effects include ACh side effects as well as CNS excitation/restlessness / irritability / sleep loss. Primary concern: Food/drug interactions related to MAO A’s role in normally breaking down tyramine (in bananas, coffee, tea, aged cheese, etc.). If tyramine is releaed into blood when taking an MAOI, stimulates a release of NE -> violent headaches, HTN, & CVA!
- Selective Serotonin Reuptake Inhibitors (SSRIs) - inhibit reuptake of serotonin to prolong its presence in the synaptic cleft. Examples include those that end with -ETINE (Fluoxetine/Proxac, Paroxetine/Paxil, Sertraline/Zoloft) and with -ALOPRAM (Citalopram/Celexa, Escitalopram/Lexapro). These have NO ACh, histamine, or adrenergic side effects because the drugs are more selective! CELEXA has even fewer drug-drug interactions. 1 NT involved = fewer side effects. May have increased risk for SI.
- Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) - these treat both depression and generalized anxiety disorder by inhibiting reuptake of SEROTONIN (at low doses) and NOREPINEPHERINE (at high doses) to prolong their presence in the synaptic cleft. Examples include Venlafxine/Effexor, Duloxetine/Cymbalta, and Desvenlafaxine/Pristiq. These have NO ACh, histamine, or adrenergic side effects because the drugs are more selective! Want to monitor for SI and changes in cardiac status (HTN). 2 NTs involved = medium amount of side effects.
Most commonly prescribed anti-epileptic is ___. It is the primary drug for all seizures EXCEPT one type of seizures: ___. It is also used with __ neuralgia. We like this one because it has no real __ side effects, which are common with other anti-epileptics! However, the metabolism is complex, so we do see side effects such as…
Most commonly prescribed anti-epileptic is DILANTIN (PHENYTOIN) . It is the primary drug for all seizures EXCEPT one type of seizures: ABSENCE. It is also used with TRIGEMINAL neuralgia. We like this one because it has no real SEDATION side effects, which are common with other anti-epileptics! However, the metabolism is complex, so we do see side effects such as:
Rashes
Excess hair growth
Hepatitis
Gingival hyperplasia (gums)
Coarsening of facial features
Systemic side effects such as HYPERglycemia, osteomalacia, cardiac (arrhythmias, HoTN) and excitatory effects on the cerebellar-vestibular system (nystagmus, ataxia, dizziness)
*Tegretol/Carbamazepine is similar; fewer cosmetic side effects but it DOES have SEDATIVE side-effects
What is the drug of choice for absence seizures? Side effects? Other uses?
VALPROATE/Depakene is the drug of choice for absence seizures (since DILANTIN doesn’t touch those), and is also effective for tonic-clonic, atonic, and myotonic seizures. Also used w/migraine prophylaxis! Side effects are related to CNS depression: drowsiness, sedation, HA etc…though these side effects are not as severe as w/other meds. Valproate acts by increasing GABA and preventing GABA reuptake at synpases.
Meds to address spasticity at a central level include… (3)
Diazepam (Valium) - binds to GABA-gated chloride channel
Baclofen (Lioresal) - decreases neurotransmitter release of monoamine, similar in nature to GABA but doesn’t bind to GABA receptors
Tizanidine (Zaniflex) -alpha 2 adrenergic agonist, greater inhibition of motor neurons
Diazepam (aka ___) is used to address spasticity [peripherally / centrally], often with the __ and __ populations. It binds to __-gated chloride channels. Side effects include [5]. Of note using [what other substances?] concurrently can increase the risk for CNS depression and apnea. Note of caution: it increases muscle ___ ___ which is concerning for balance reactions!
Diazepam (aka VALIUM) is used to address spasticity CENTRALLY, often with the SCI and CP populations. It binds to GABA-gated chloride channels - it’s a benzo! Side effects include DROWSINESS, FATIGUE, ATAXIA, DEPRESSION, and RISK OF APNEA Of note using BARBITUATES, EtOH, or other CNS DEPRESSANTS concurrently can increase the risk for CNS depression and apnea. Note of caution: it increases MUSCLE RESPONSE TIME which is concerning for balance reactions!
Oral baclofen is a [central / peripheral] anti-___ agent which is often used in what populations (2)? What populations is intrathecal baclofen used with?
Side effects of baclofen include CNS [excitation / depression], __, __, and __ and __ depression. We see additive side effects when it is used concurrently with __ or __. Sudden withdrawal may result in __ or __.
Oral baclofen is a CENTRAL ANTI-SPASTICITY agent which is often used in MS and SCI. Intrathecal baclofen is used in MS, SCI, and CVA. Can also use w/TBI, but encourage you to wait ~1 year prior to implanting ITB pump.
Side effects of baclofen include CNS DEPRESSION, ATAXIA, SOMNOLENCE, CARDIAC and RESPIRATORY depression. We see additive side effects when it is used concurrently with EtOH or other CNS DEPRESSANTS. Sudden withdrawal may result in SEIZURE or HALLUCINATION.
Of note, baclofen may reveal (or lead to) increased muscle weakness.
Tizanidine (aka ___) is a [central / peripheral] anti-___ med which is a(n) [alpha / beta ] [ 1 / 2] adrenergic [agonist / antagonist] which increases [excitation/inhibition] of motor neurons. It is used in [3] populations and may be tolerated [worse / better ] than a benzo (i.e. which drug?) or ITB and is less likely to show muscle weakness. This drug can also be used to [increase / reduce] blood pressure! BIG side effect you need to watch out for is ___, with onset as soon as ___ minutes/hour/days post-administration, and peak at ___ minutes/hour/days post. Other side effects include __, ___, __, or __.
Tizanidine (aka ZANAFLEX) is a CENTRAL anti-SPASTICITY med which is a(n) ALPHA-2 adrenergic AGONIST which increases INHIBITION of motor neurons. It is used in MS, SCI, and CVA populations and may be tolerated BETTER than a benzo (i.e. DIAZEPAM) or ITB and is less likely to show muscle weakness. This drug can also be used to DECREASE blood pressure! BIG side effect you need to watch out for is HoTN, with onset as soon as 1 HOUR post-administration, and peak at 2-3 HOURS post. Other side effects include SOMNOLENCE, ASTHENIA (abnormal weakness), DIZZINESS, or DRY MOUTH.
Peripheral anti-spasticity agents include __ and __. Which is better for use with widespread spasticity?
Peripheral anti-spasticity agents include DANTROLENE SODIUM (DANTRIUM) and BOTOX TYPE A. DANTRIUM is better for use with widespread spasticity, and is used in CVA, MS, and CP populations, vs botox is also helpful in brain injury, SCI and neurodegenerative diseases for focal spasticity
Dantrolene sodium (aka __) is a(n) [central / peripheral] anti-___ medication that works by altering the excitation-contraction coupling by interfering with [anion] flux at the [part of the muscle fiber]. It affects [fast / slow] twitch muscle fibers more but is good for use with [focal / widespread] spasticity in the (3) populations. CNS side effects include __, __, and __ but you also need to monitor __ function (particularly in [males / females] over the age of ___, and in those at high doses)
Dantrolene sodium (aka DANTRIUM) is a PERIPHERAL anti-SPASTICITY medication that works by altering the excitation-contraction coupling by interfering with CALCIUM flux at the SARCOPLASMIC RETICULUM. It affects FAST TWITCH twitch muscle fibers more than slow twitch, but is good for use with WIDESPREAD spasticity in the MS, CVA, and CP populations. CNS side effects include DROWSINESS, DIZZINESS, and GENERALIZED WEAKNESS but you also need to monitor LIVER function (particularly in FEMALES over the age of 45, and in those at high doses)
Botulinum Toxin Type A (aka ___ ) is a(n) [central / peripheral] anti-___ medication that works by blocking the release of __ at the neuromuscular junction, thereby blocking muscular contraction. Side effects include muscle ___ both locally and to other muscles, spreading via ___ transmission. Once delivered, it acts within __-__ minutes/hours/days, but may require reinjection due to collateral growth/new nerve junctions for longer results. Lasts __-__ minutes/ days/ weeks/ months/ years, but you can develop __ and __ to it over time! May make [agonist/antagonist] muscle weakness more evident. PT modalities at the injection site are contraindicated x____minutes/hours/days/weeks
Botulinum Toxin Type A (aka BOTOX A ) is a PERIPHERAL anti-SPASTICITY medication that works by blocking the release of ACETYLCHOLINE at the neuromuscular junction, thereby blocking muscular contraction. Side effects include muscle WEAKNESS both locally and to other muscles, spreading via RETROGRADE transmission. Once delivered, it acts within 24-48 HOURS, but may require reinjection due to collateral growth/new nerve junctions for longer results. Lasts 3-8 MONTHS, but you can develop ANTIBODIES and IMMUNITY to it over time! May make ANTAGONIST muscle weakness more evident. PT modalities at the injection site are contraindicated 10 DAYS
The presence of [excitatory/inhibatory] glutamate is thought to be related to seizure activity in the brain. Therefore, the pharmacological focus is to augment inhibitory activity of [neurotransmitter] OR by blocking [ion] and [ion] channels.
The presence of EXCITATORY glutamate is thought to be related to seizure activity in the brain. Therefore, the pharmacological focus is to augment inhibitory activity of GABA OR by blocking Na+ or Ca++ channels.
