CNS Drugs Flashcards
cerebrum
thinking, preception, speech, memory, smell
thalamus
relay center for sound, sight, pain ,tough, tempwerature, controls mood/ motivation
cererbellum
controld muscle movement, postrue, tone
brainstem
connects spinal cord to brain, medullla oblongata, pons/midbrain
reflex/controlc enter, breathing, heart rate, swallowing, coughing, vominting, vosion
spinal cord
transmits to and from brain
parasthesia
numness/ tingling in responset o spinal cord injury
paralysis
immobilazation due to spinal cord injury
limbi system
controls behavior, emotions, feeling, also containg basal ganglia with fin tuned sensory
reticular activating sysstem
controls ability to tune repetitive sensaation out
blood brain barrier
protect from pathogens/ toxins, supplies oxygen, glucose, nutrients
specifications of a drug to pass the blood brain barrier
ForCNS drugs, lipid soluble, not protein bound, low ionized
neuron transmission
cell body of neuron becomes stimulated- send signal down axon covered myelin sheath- signal transmitted at synapse of next neuron
opiod peptides
endogenous painkillers that th ebody makes
Blockiiin greuptake of neurotransmitters
a drug action of drugs that stop neurotransmitters from going back up the axon and being reabsrobed which causes an increased concentration of neurotransmitters sittin gin the presynaptic membrane
4 actions od drugs
blocking reuptake of neurotransmitters
blocking enzymes that break down neurotransmitters
stimulating specfic receptor sites when neurotransmitters are unavoidable
stimulate presynaptic nerve to realse increased amounts of NT
What is pain
whatever the person expirenceing it says it is
pain transduction
injured tissues release neurotransmitters connected to pain- NT stimulate nociceptors in skin, connective, tissue, muscle, circulatroy system, throacic, abdomen, pelvis
pain transmission
pain stimul entering spinal cord in dorsal horn
substance p released in respons to paiun thats acts a neurotransmitter hand has a role in interpreting pain and determing self analghesis response
substance p
neuropeptide released in response to pain
pain perception
pain impulse reaches brain- now conscious awareness of pain
pain modulation
reaction/regulation/inhibition
seratonin/neurotensin bring pain down
GABA calming, endogenous opioids
Opioid receptors
kappa and mu
how is main modulated at opioid receptors
endogenous opioids can activate these receptors, also where exoghenous opioids work. If they are not blocked, signal moves to thalamus in brain
Responses to an activates Mu receptor
analgesic, respiratoy depression, sedation,euphroa, physical dependence, decreased gi motility
responses to a activated kappa receptor
analgesic, sedation, decreased GI motility
inhibitory substances
released in synapse, bind with opioid receptors on dorsal horn and prevent further transmission of pain
nociceptive pain
somatic (deep) visceral pain
acute pain
lasts 3-6mo physical cause like soft tissue damgae that can be treated
signs of acute pain
hypoxia, hypercapnia, hypertension, tachycardia, emotional difficulties
chronic pain
last longer than 6 mo, left over of an injury or from cancer or other unidetifyable cause
neuropathic pain
caused by other disease, like diabetes
vascular pain
interupption of blood flow, lack of circulation
heaviness, numbness, tingling
psychogenic pain
caused by underlying psych factors
reffered pain
pain is felt in one are but actual injuiry is in another area
results of unrelieved pain
stress hormone response, impaired muscle movementm changes in quality of life
pain assessment
location, severity, type, duration, effects on ADLs
opiate
compounds present in opium, morphein, codeine, heroin
opioid
any drug that has actions similar to those of morphine, vicodin, oxycodone, fentanyl
opioid agonists (activation)
activate mu and kappa
mixed opioid agonists-antagonists
block mu/kappa and activate other site
opioid antagonist
block both mu and kappa
Strong narcotic agents
p-morphine
fentanyl
hydromorphone
meperidine
methadone
oxycodone
Stronmg narcotic agents MOA
occupies mu and kappa in brain and dorsal horn which reduced the release of neurotransmitter, preventing the transmission of nociceptor pain
therapeutic uses of morphine
pain: post surgical, sever pain from trauma/disease, cancer
coughing
sever diarrrhea
morphine kinetics
not very lipid soluble- does not cross blood brain barrier very easily
why are morphine doses higher orally
high first pass effect, only a small fraction reaches site of analgesisc action
where is morphine metabolized
liver
where is morphine eliminated
kidneys and feces
number 1 risk with morphine use
respiratory depression
who is most at risk for respiratory depression with morphine
infants/elderly
resp depression with IV morphine onset
7 min
resp depression with IM morphine onset
30 min
resp depression with SQ morphine onset
90 min
under what resp condition should you hold morphine
RR under 12 breath pm
what sign of resp depression does morphine present
decreased resp rate, resp arrest, apnea
treating morphine overdose
naloxone
what can increase risk of morphine related resp depression
concurrent us with other CNS depressant drugs
risks of using morphine to help with cough
accumulation of secretion, ,may put patient at higher risk of aspiration
how does morphine cause constipation
suppresses GI peristalsis and decreases secretion of fluis in intesttines
morphine causing emesis
simulates chemoreceptor trigger zone in medulla, geatest with initial dose and then diminishes
how does mophine cause biliary colic
induces spasma of the common bile duct, causing epigastric distress
use meperedine to induce less muscle spasms
morphine effecting cardiovascular
lower BP by dilating blood vesseld and may blunt baroreceptro reflexes,
orhtostatic hypotension
morphine and GU
causes retention and hesitancy
increased bladder pressure- sense of urgency
increased tone of bladder sphincter
morphine on ICP
suppresses respiration- co2 increases-dilates vessels in brain- ICP rise
morphine and euphoria
morphine binding to mu receptors
enhances pain relief, adds to potential for abuse
morphine and sedation
drowsiness and mental clouding
avoid hazardous activities
minimize with lower doses, shorter half lives
morphine and eyes/skin
miosis, uticaria
when are opioids contraindicated
resp depression, pts receiving other CNS depressants, alcoholics/addicts, heady injury, hypersensitivity, pregnancy
what drugs can interact with opioid
any other hepatically cleared drug
what drugs should be used with caution with morphine
hypotensive drugs, CNS depressants (alcohol)
possible results of opioir drug interactions
sedation, respiratoy depression
pain med or hypertensive med first
pain med, as it can increase BP
What med schedule is the best for staying on top of pain
PCA>fixed schedule> PRN
Moderate Narcotic Agonists
P-Codeine, Hydrocodone (vicodin), oxycodone (oxycontin)
Codeine MOA
acts at opioid receptors in CNS to produce analgesia, euphoria, sedation
acts on medullary cough center to depress cough reflex
drying effect on mucous membrane
adverse effects of codeine as cugh suppressant
dry mouth, drowsiness, sedation, if analgesis similar effects as morphine
NArcotic agonists- antagonists
P-Pentazocine (Talwinn), buprenophine, butorphanol, nalbuphine
opioid antagonist
have high affinity for opioid receptor but cause no effect
Naloxone (narcan)
possible side effects of opioid antagonist
hypot/hyper tension
Tolerance
body becomes accustomed to effect of the substance, must use more to get desired effect
develops to analgesia, respratory, euphoria, not miosis, constipation
dependence
withdrawal symptoms when drug discontinued
physiologi, not psych
addiction
compulsive use of drug for secondary gain, not for pain control
psych
symptoms of opioid withdrawal
sweating, runny nose, ittitability, tremr, anorexia, nausea/vomiting, diarrhea, cramps, muscle spasms
how to treat pain with opioids
start with low dose and titrate up
around the clock better than prn
Adjuvant drugs
assist primary drugs in relieveing pains
NSAIDs, ANtidepressants, anticonvulsants, corticosteroids
For which patient would codeine be contraindicated?
* A. Postoperative patient with chest tubes
* B. Postoperative patient with pain after ORIF of left arm
* C. Patient with mild-to-moderate pain after breaking right
tibia
* D. Patient who has nonproductive cough that is
preventing normal sleep
A, codeine can help suppress cough, but cough should be encouraged with chest tubes
classic signs of inflammation
heat, redness, swelling, pain, loss of function
inflammation vascular response
immediately after injury
vasoconstriction in surroudning tissues, than vasodilation to increase blood flow to injury
cap permiabilit increases so fluid accumulates in tissue, and chemical mediators released causing pain and malfunction
Inflammaition cellular response
WBS move to periphary of blood vesssels- pass into tissue spaces- cell debris/bacteria attract to WBCs- engulfed by WBCs
inflammation chemical response
mast cells rupture and release biochemical mediators which contribute to inflammation
Prostaglandins
regulate inflammation, body temp, pain transmission, platelet aggregation, Gi protection
how is prostaglandin formed
acid released from cell membrane converted by cyclooxygenase (COX) enzyme into prostaglandin
what do prostaglandins do
increase uterine/smooth muscle contractions
decrease BP
decrease gastric acid secretion
increase mucus production
increase body temp
increase platelet aggregation
increase renal vasodilation
increase inflammation and capillary permeability
“Good” COX 1
produces prostaglandins involved in regulating normal cell activity
“bad” COX 2
produces prostaglandins at sites of inflammation
actions of COX 1
normal cell activity, protects GI, regulated smooth muscles, normal renal function, promotes plt aggregation
actions of COX 2
sensitizes pain, increases fever, inflammation, increases cap permeability, contribute to colon cancer
results of inhibiting COX1
GI ulcers/bleeding, increased bleeding, renal impairment, bronchoconstriction, HTN
MI/Stroke protection
results of inhibting COX2
decreased inflammation, decreased pain, decreased fever, protect again colon cancer
increased vasoconstriction, risk of MI/Stroke
what do first generation NSAIDS do
inhibti COX 1/2
treat inflammatory disorders, alleviate mild to moderate pain, suppress fever, relieve dysmenorrhea
suppress inflammation
salicyclates
first gen NSAID
P-aspirin
Aspirin MOA
non selective inhibitor of cyclooxygenase
Asprin therapeutic uses
analgesic
antipyretic, anti inflammatory, anti platelet, dysmenorrhea, cancer prevention, alzhemiers prevention
aspirin as anti-pyretic
works on hypothalmus
aspirin anti inflammatory
inhibits COX- inhibts prostaglandin synthesis
asprin alagesis
inhibits cox-inhibits prsotaglandins that sensitize pain receptors
aspirin antiplateleet
inhibits Thromboxane A2- prostaglandin that induces platelet aggregation
Aspirin kinetics
mostly absorbed in small intestine, usually within 30 minutes depending on form, gastric pH, food
aspirin side effects
GI bleed, renal impairnment, tinnitus, hypersensitvity, reyes syndrome
reyes syndrome
giving aspirin to a young child for a fever may cause encephalopy/liver damage
aspirin hypersensitivity reaction
tinnitus, vertigo, bronchospasm
more likely with nasal polyps
avoid diflinisal if hypersensitive
contraindications with Aspirin
peptic ulcer/ bleeding disorder, with anti coagulation therapy, gout/renal/liver pt, children with fllu symptoms/fever, caution with smokers/ w/ alcohol
aspirin in prgnanacy
cat C in 1st/2nd trimester
cat D in 3rd trimester
Salicylism
asprin toxicity typically with long term/high dose therapy
mild aspirin toxicity
> 200 mcg/ml
severe aspirin toxicity
> 400 mcg/mL
s&s of salicylism
headahce, tinnitus,, GI distress, respiratoy stimulation, drowsiness/confusion
treatment of salicylism
dose reduction, halting of therapy
Salicylate poisoning
life threatening, with no anditote
same s&s, just more and quicker
treat with gstric emptying and life support
prostaglandin synthetase inhibitors
first GEN NSAIds
P-ibuprophen
naproxen (aleve), indomethacin (indocin), ketorolac (toradol)
ibuprophen MOA
inhibit COX 1/2
ibuprohpne kinetics
amsorbed in GI, slower if with food
analgesis/antipyretic effects 2-4 hrs
inflammatroy nedd higher dose and few day-weeks
highly protein bound
contrainidcation/cautions of ibuprophen
ulcer/bleeding disorder pts
heart pts
renal pateint- inhibition of renal prostaglandins can decrease renal blood flow
ibuprofen black box warning
serious GI events
increased risk of cardiovascular thrombotic events
second- generation NSAIDs
suppressing inflammatio/pain, with lower risk of GI side effects
can impair renal function, cause hypertension/edema, increase MI/Stroke risk
selectinve COX-2 ihibitors
2nd gen NSAID
P-celecoxib (celebrex)
cannot use if sulfa allergy
celecoxib MOa
inhibit COX-2 enzyme, inhibits prostaglandin synthesis
Celecoxib indications
arthrits, acute pain, dymenorrhea
celecoxib side effects
dyspepsia, abdominal pain, sulonamide allergy, increase risk of stroke, mi, other CV event
para-aminophenol Derivatives
p-acetaminophen
acetaminophen MOA (fever)
direct action on hypothalamic heat regulatin center, inhibg action of chemical that cuses vasodilation and sweating
acetaminophen MOA (pain)
unclear, but not anti inflammayory effect or platelet aggregation inhibition
inhibit prostaglandin synthesis in CNS
Acetaminophen indications
Fever, mild to moderate pain
no anti-inflammatory
drug of choice for infants, pregnancy
acetaminophen kinetics
absorbed: rapidly and orally
distributed: onset 30 min, peak 1-2 hrs, duration 4 hrs
metabolized : liver
exreted: kidneys
acetompinophen side effects
rash uticaria, nausea, fever, neutropenia, thrombocytopenia, jaundice, hepatotoxicity, hepatic necrosis
all Rare
acetompinophen interaction
caution w/ hepatic disease/ other drugs that could cause liver damage
may axacerbate anemias
acetominophen contradiction
hepatic disease, viral hepatitis, alcoholism
acetominophen overdose
glutathione, which converts toxic metabolit into nontoxic, quickly depleted in overdose.
accumulation occurs, equals liver damage
S&S acetominophen overdose
anorexia, nausea/vomiting, pallor, abdominal discomfort, jaundice
acetominophen antidite
acetylcysteine
