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87 Cards in this Set
- Front
- Back
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CNS drugs |
agents that act on the brain and spinal cord |
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medical uses for CNS drugs |
relief of pain suppression of seizures production of anesthesia treatment of psychiatric disorders |
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nonmedical uses of CNS drugs |
stimulant depressant euphoriant mind altering abilities |
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plausible hypothesis and CNS drugs |
cannot state with certainty how CNS drugs act, do not have sufficient data to form a plausible hypothesis |
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drugs and chronic timing |
certain drugs must be taken for several weeks before full therapeutic effects develop |
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adaptation |
when CNS drugs are taken chronically, intensity of side effects may decrease but the therapeutic effects remain undiminished |
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tolerance |
decreased response occurring during the course of prolonged use |
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physical dependence |
state in which abrupt disruption of drug use with cause a withdrawal syndrome must be tapered off |
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addiction |
mental health diagnosis for drug-seeking behavior |
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what can pass BBB? |
lipid soluble drugs |
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BBB in newborns and children |
not fully developed and must be careful |
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what is parkinson's disease? |
neurodegenerative disorder associated with disruption of neurotransmission |
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symptoms of PK |
dysknisias- tremors, posture imbalance, rigidity, bradykinisia akynisias- no movement |
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neurofunction behind PK |
imbalance of dopamine and ACh less dopamine |
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what drug is used for mild symptoms of PK? |
MAO-B inhibitor Selegiline |
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what drug is used for more severe symptoms of PK? |
levodopa combined with carbidopa |
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what drugs are used for "off times" with PK? |
dopamine agonists COMT inhibitors MAO-B inhibitors |
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2 categories of drugs for PK |
dopaminergic anticholinergic |
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dopaminergic agents and PK |
bring more dopamine to CNS most common levodopa/carbidopa |
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anitcholinergic agents and PK |
against ACh to balance with dopamine prevent activation of cholinergic receptors |
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types of dopaminergic agents |
levodopa- promotes dopamine synthesis dopamine agonists- stimulate dopamine receptors COMT inhibitors- block degeneration of levadopa MAO-inhibitors- block inactivation of dopamine |
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what is Alzheimer's disease? |
progressive memory loss |
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what internally happens with AD? |
degeneration of neurons -early in hippocampus (memory) -later in cerebral cortex (speech, perception, reasoning) -plaques, tangles, tau |
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what is an internal factor with AD? |
levels of ACh drop below normal |
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symptoms of AD and age |
typically begin after 65 but can begin at 40 |
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effectiveness of AD drugs |
cannot help very much |
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categories of drugs with AD |
cholinesterase inhbitors NMDA inhibitors |
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cholinesterase inhibitors and AD |
inhibit breakdown of ACh, increase transmission ineffective if ACh is not present Donepezil |
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NMDA receptor inhibitors and AD |
block neuronal receptors for NMDA Memantine |
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what is multiple sclerosis? |
chronic, inflammatory autoimmune disorder that damages myelin sheaths |
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cause of MS |
unknown |
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4 types of MS |
relapsing remitting secondary progressive primary progressive progressive relapsing |
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relapsing remitting MS |
reucrrent, clearly defined episodes followed by periods of recovery |
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secondary progressive MS |
relapsing-remitting steadily intensifies |
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primary progressive MS |
more intense, may experience temporary plateau or temporary improvement |
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progressive relapsing MS |
acute exacerbations with steady intensification of symptoms |
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drug therapy categories for MS |
immunomodulators immunosuppressants |
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immunomodulators for MS |
interferon beta |
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immunisuppressants for MS |
mitoxantrone |
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what is epilepsy? |
excessive exciteability of neurons in CNS |
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simple partial epilepsy |
no loss of consciousness twitching |
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complex partial epilepsy |
impaired consciousness |
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secondary generalized epilepsy |
start with absence or twitches, turns into tonic-clonic convulsions |
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problem with side effects and drugs with epilepsy |
must balance complete seizure control with side effects |
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how many epileptics are able to be treated successfully? |
2/3 |
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for 1/3 of non-treatable epileptics, what works? |
neurosurgery vagus nerve stimulation ketogenic diet |
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epileptic drug evaluation |
trial period monitor plasma drug levels (for tonic clonic because they are infrequent) if symptoms remiss, withdraw slowly monitor for suicidal behaviors |
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pregnancy and epilepsy |
consideration to continuing medication, but AVOID VALPROIC ACID |
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AE drug effects |
suppress discharge of neurons within a seizure focus suppress Na influx, Ca2+ influx, inhibit glutamate, potentiate GABA to decrease exciteability |
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traditional AED |
phenytoin carbamazepine valproic acid ethosuximide phenobarbita diazepam |
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newer AED |
oxcarbazepine lamotrigine gabapentin |
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therapeutic window is narrow for what AE drug? |
phenytoin |
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selegine should never be mixed with |
meperidine |
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unique aspect of glatiramer acetate |
10% of pt have postinjection reaction flushing, palpitations, sever chest pain, anxiety, laryngeal, constriction, urticaria (wheels and itching) |
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what is glatiramer acetate used to treat? |
MS |
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most dangerous anti-epileptic for pregnant women? |
valproic acid |
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valproic acid should not be taken with |
phenytoin |
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muscle spasms are treated with... |
centrally-acting muscle relaxants |
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spasticity is treated with... |
baclofen diazepam dantrolene |
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spasticity is due to |
originates in CNS often due to MS cerebral palsy spinal cord injury |
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all centrally acting muscle relaxants produce |
generalized CNS depression |
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function of local anesthetics |
suppress pain by blocking Na channels and blocking impulse conduction along axon suppresses pain without generalized depression of CNS |
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basic adverse effects of local anesthetics |
CNS- excitation followed by depression CV- bradycardia, heart block, decreased contractile force, cardiac arrest, hypotension allergic reactions methehemoglobihemia- prevent O2 from leaving RBC prolong labor |
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2 major groups of local anesthesia |
esters-procaine amides- lidocaine |
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local anisthetics are selective/non-selective? |
non-selective |
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gradual effects of local anesthetics |
pain cold warmth touch deep pressure |
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what is used with local anisthetics to prolong effects? |
vasoconstrictors (epinephrine) |
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never put epi in |
fingers toes noses penises |
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where can topical admin of local anesthetics be applied? |
skin mucous membranes |
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prevention of systemic toxicity with local anesthetics |
can cause depression of CNS and bodily functions -apply smallest amount needed -small area only -don't wrap or apply heat to slide |
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types of injection admin of local anesthetics |
infiltration nerve block intravenous regional epidural spinal (subarachnoid) |
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inflitration injection admin of local anesthetic |
inject directly into site, usually with epi |
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nerve block admin of local anesthetic |
inject into nerve distal to target |
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intravenous regionaladmin of local anesthetic |
inject into vein of arm/leg after tourniquet |
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epiduraladmin of local anesthetic |
into epidural space (inside spinal column but outside dura mater) |
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spinal admin of local anesthetic |
into subarachnoid space adverse effect- hypotension |
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analgelsic |
drug that relieves pain without causing loss of consciousness |
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opioid |
any drug that has actions similar to those of morphine |
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opiate |
applies to only compounds present in opium |
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what to watch when giving opioids |
respirations |
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mu receptor effects when activated |
analgesia respiratory depression euphoria sedation physical dependence |
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classifications of drugs that act at opioid receptors |
pure opioid agonists agonist-antagonist opioids pure opioid antagonists |
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pure opioid agonists |
activate mu and kappa receptors |
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agonist-antagonist opioids |
administered alone, produce analgesia administered with opioid, can help reverse anagelsia and adverse effects |
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pure opioid antagonists |
inhibit mu and kappa receptors |
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because morphine can cause constipation... |
may use along with stool softener may be used by patient with diarrhea |
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morphine and head injury |
NONO because increases intracranial pressure |
