CNS Drugs Flashcards
1
Q
cerebrum
A
thinking, preception, speech, memory, smell
2
Q
thalamus
A
relay center for sound, sight, pain ,tough, tempwerature, controls mood/ motivation
3
Q
cererbellum
A
controld muscle movement, postrue, tone
4
Q
brainstem
A
connects spinal cord to brain, medullla oblongata, pons/midbrain
reflex/controlc enter, breathing, heart rate, swallowing, coughing, vominting, vosion
5
Q
spinal cord
A
transmits to and from brain
6
Q
parasthesia
A
numness/ tingling in responset o spinal cord injury
7
Q
paralysis
A
immobilazation due to spinal cord injury
8
Q
limbi system
A
controls behavior, emotions, feeling, also containg basal ganglia with fin tuned sensory
9
Q
reticular activating sysstem
A
controls ability to tune repetitive sensaation out
10
Q
blood brain barrier
A
protect from pathogens/ toxins, supplies oxygen, glucose, nutrients
11
Q
specifications of a drug to pass the blood brain barrier
A
ForCNS drugs, lipid soluble, not protein bound, low ionized
12
Q
neuron transmission
A
cell body of neuron becomes stimulated- send signal down axon covered myelin sheath- signal transmitted at synapse of next neuron
13
Q
opiod peptides
A
endogenous painkillers that th ebody makes
14
Q
Blockiiin greuptake of neurotransmitters
A
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
15
Q
4 actions od drugs
A
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
16
Q
What is pain
A
whatever the person expirenceing it says it is
17
Q
pain transduction
A
injured tissues release neurotransmitters connected to pain- NT stimulate nociceptors in skin, connective, tissue, muscle, circulatroy system, throacic, abdomen, pelvis
18
Q
pain transmission
A
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
19
Q
substance p
A
neuropeptide released in response to pain
20
Q
pain perception
A
pain impulse reaches brain- now conscious awareness of pain
21
Q
pain modulation
A
reaction/regulation/inhibition
seratonin/neurotensin bring pain down
GABA calming, endogenous opioids
22
Q
Opioid receptors
A
kappa and mu
23
Q
how is main modulated at opioid receptors
A
endogenous opioids can activate these receptors, also where exoghenous opioids work. If they are not blocked, signal moves to thalamus in brain
24
Q
Responses to an activates Mu receptor
A
analgesic, respiratoy depression, sedation,euphroa, physical dependence, decreased gi motility
25
responses to a activated kappa receptor
analgesic, sedation, decreased GI motility
26
inhibitory substances
released in synapse, bind with opioid receptors on dorsal horn and prevent further transmission of pain
27
nociceptive pain
somatic (deep) visceral pain
28
acute pain
lasts 3-6mo physical cause like soft tissue damgae that can be treated
29
signs of acute pain
hypoxia, hypercapnia, hypertension, tachycardia, emotional difficulties
30
chronic pain
last longer than 6 mo, left over of an injury or from cancer or other unidetifyable cause
31
neuropathic pain
caused by other disease, like diabetes
32
vascular pain
interupption of blood flow, lack of circulation
heaviness, numbness, tingling
33
psychogenic pain
caused by underlying psych factors
34
reffered pain
pain is felt in one are but actual injuiry is in another area
35
results of unrelieved pain
stress hormone response, impaired muscle movementm changes in quality of life
36
pain assessment
location, severity, type, duration, effects on ADLs
37
opiate
compounds present in opium, morphein, codeine, heroin
38
opioid
any drug that has actions similar to those of morphine, vicodin, oxycodone, fentanyl
39
opioid agonists (activation)
activate mu and kappa
40
mixed opioid agonists-antagonists
block mu/kappa and activate other site
41
opioid antagonist
block both mu and kappa
42
Strong narcotic agents
p-morphine
fentanyl
hydromorphone
meperidine
methadone
oxycodone
43
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
44
therapeutic uses of morphine
pain: post surgical, sever pain from trauma/disease, cancer
coughing
sever diarrrhea
45
morphine kinetics
not very lipid soluble- does not cross blood brain barrier very easily
46
why are morphine doses higher orally
high first pass effect, only a small fraction reaches site of analgesisc action
47
where is morphine metabolized
liver
48
where is morphine eliminated
kidneys and feces
49
number 1 risk with morphine use
respiratory depression
50
who is most at risk for respiratory depression with morphine
infants/elderly
51
resp depression with IV morphine onset
7 min
52
resp depression with IM morphine onset
30 min
53
resp depression with SQ morphine onset
90 min
54
under what resp condition should you hold morphine
RR under 12 breath pm
55
what sign of resp depression does morphine present
decreased resp rate, resp arrest, apnea
56
treating morphine overdose
naloxone
57
what can increase risk of morphine related resp depression
concurrent us with other CNS depressant drugs
58
risks of using morphine to help with cough
accumulation of secretion, ,may put patient at higher risk of aspiration
59
how does morphine cause constipation
suppresses GI peristalsis and decreases secretion of fluis in intesttines
60
morphine causing emesis
simulates chemoreceptor trigger zone in medulla, geatest with initial dose and then diminishes
61
how does mophine cause biliary colic
induces spasma of the common bile duct, causing epigastric distress
use meperedine to induce less muscle spasms
62
morphine effecting cardiovascular
lower BP by dilating blood vesseld and may blunt baroreceptro reflexes,
orhtostatic hypotension
63
morphine and GU
causes retention and hesitancy
increased bladder pressure- sense of urgency
increased tone of bladder sphincter
64
morphine on ICP
suppresses respiration- co2 increases-dilates vessels in brain- ICP rise
65
morphine and euphoria
morphine binding to mu receptors
enhances pain relief, adds to potential for abuse
66
morphine and sedation
drowsiness and mental clouding
avoid hazardous activities
minimize with lower doses, shorter half lives
67
morphine and eyes/skin
miosis, uticaria
68
when are opioids contraindicated
resp depression, pts receiving other CNS depressants, alcoholics/addicts, heady injury, hypersensitivity, pregnancy
69
what drugs can interact with opioid
any other hepatically cleared drug
70
what drugs should be used with caution with morphine
hypotensive drugs, CNS depressants (alcohol)
71
possible results of opioir drug interactions
sedation, respiratoy depression
72
pain med or hypertensive med first
pain med, as it can increase BP
73
What med schedule is the best for staying on top of pain
PCA>fixed schedule> PRN
74
Moderate Narcotic Agonists
P-Codeine, Hydrocodone (vicodin), oxycodone (oxycontin)
75
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
76
adverse effects of codeine as cugh suppressant
dry mouth, drowsiness, sedation, if analgesis similar effects as morphine
77
NArcotic agonists- antagonists
P-Pentazocine (Talwinn), buprenophine, butorphanol, nalbuphine
78
opioid antagonist
have high affinity for opioid receptor but cause no effect
Naloxone (narcan)
79
possible side effects of opioid antagonist
hypot/hyper tension
80
Tolerance
body becomes accustomed to effect of the substance, must use more to get desired effect
develops to analgesia, respratory, euphoria, not miosis, constipation
81
dependence
withdrawal symptoms when drug discontinued
physiologi, not psych
82
addiction
compulsive use of drug for secondary gain, not for pain control
psych
83
symptoms of opioid withdrawal
sweating, runny nose, ittitability, tremr, anorexia, nausea/vomiting, diarrhea, cramps, muscle spasms
84
how to treat pain with opioids
start with low dose and titrate up
around the clock better than prn
85
Adjuvant drugs
assist primary drugs in relieveing pains
NSAIDs, ANtidepressants, anticonvulsants, corticosteroids
86
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
87
classic signs of inflammation
heat, redness, swelling, pain, loss of function
88
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
89
Inflammaition cellular response
WBS move to periphary of blood vesssels- pass into tissue spaces- cell debris/bacteria attract to WBCs- engulfed by WBCs
90
inflammation chemical response
mast cells rupture and release biochemical mediators which contribute to inflammation
91
Prostaglandins
regulate inflammation, body temp, pain transmission, platelet aggregation, Gi protection
92
how is prostaglandin formed
acid released from cell membrane converted by cyclooxygenase (COX) enzyme into prostaglandin
93
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
94
"Good" COX 1
produces prostaglandins involved in regulating normal cell activity
95
"bad" COX 2
produces prostaglandins at sites of inflammation
96
actions of COX 1
normal cell activity, protects GI, regulated smooth muscles, normal renal function, promotes plt aggregation
97
actions of COX 2
sensitizes pain, increases fever, inflammation, increases cap permeability, contribute to colon cancer
98
results of inhibiting COX1
GI ulcers/bleeding, increased bleeding, renal impairment, bronchoconstriction, HTN
MI/Stroke protection
99
results of inhibting COX2
decreased inflammation, decreased pain, decreased fever, protect again colon cancer
increased vasoconstriction, risk of MI/Stroke
100
what do first generation NSAIDS do
inhibti COX 1/2
treat inflammatory disorders, alleviate mild to moderate pain, suppress fever, relieve dysmenorrhea
suppress inflammation
101
salicyclates
first gen NSAID
P-aspirin
102
Aspirin MOA
non selective inhibitor of cyclooxygenase
103
Asprin therapeutic uses
analgesic
antipyretic, anti inflammatory, anti platelet, dysmenorrhea, cancer prevention, alzhemiers prevention
104
aspirin as anti-pyretic
works on hypothalmus
105
aspirin anti inflammatory
inhibits COX- inhibts prostaglandin synthesis
106
asprin alagesis
inhibits cox-inhibits prsotaglandins that sensitize pain receptors
107
aspirin antiplateleet
inhibits Thromboxane A2- prostaglandin that induces platelet aggregation
108
Aspirin kinetics
mostly absorbed in small intestine, usually within 30 minutes depending on form, gastric pH, food
109
aspirin side effects
GI bleed, renal impairnment, tinnitus, hypersensitvity, reyes syndrome
110
reyes syndrome
giving aspirin to a young child for a fever may cause encephalopy/liver damage
111
aspirin hypersensitivity reaction
tinnitus, vertigo, bronchospasm
more likely with nasal polyps
avoid diflinisal if hypersensitive
112
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
113
aspirin in prgnanacy
cat C in 1st/2nd trimester
cat D in 3rd trimester
114
Salicylism
asprin toxicity typically with long term/high dose therapy
115
mild aspirin toxicity
>200 mcg/ml
116
severe aspirin toxicity
>400 mcg/mL
117
s&s of salicylism
headahce, tinnitus,, GI distress, respiratoy stimulation, drowsiness/confusion
118
treatment of salicylism
dose reduction, halting of therapy
119
Salicylate poisoning
life threatening, with no anditote
same s&s, just more and quicker
treat with gstric emptying and life support
120
prostaglandin synthetase inhibitors
first GEN NSAIds
P-ibuprophen
naproxen (aleve), indomethacin (indocin), ketorolac (toradol)
121
ibuprophen MOA
inhibit COX 1/2
122
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
123
contrainidcation/cautions of ibuprophen
ulcer/bleeding disorder pts
heart pts
renal pateint- inhibition of renal prostaglandins can decrease renal blood flow
124
ibuprofen black box warning
serious GI events
increased risk of cardiovascular thrombotic events
125
second- generation NSAIDs
suppressing inflammatio/pain, with lower risk of GI side effects
can impair renal function, cause hypertension/edema, increase MI/Stroke risk
126
selectinve COX-2 ihibitors
2nd gen NSAID
P-celecoxib (celebrex)
cannot use if sulfa allergy
127
celecoxib MOa
inhibit COX-2 enzyme, inhibits prostaglandin synthesis
128
Celecoxib indications
arthrits, acute pain, dymenorrhea
129
celecoxib side effects
dyspepsia, abdominal pain, sulonamide allergy, increase risk of stroke, mi, other CV event
130
para-aminophenol Derivatives
p-acetaminophen
131
acetaminophen MOA (fever)
direct action on hypothalamic heat regulatin center, inhibg action of chemical that cuses vasodilation and sweating
132
acetaminophen MOA (pain)
unclear, but not anti inflammayory effect or platelet aggregation inhibition
inhibit prostaglandin synthesis in CNS
133
Acetaminophen indications
Fever, mild to moderate pain
no anti-inflammatory
drug of choice for infants, pregnancy
134
acetaminophen kinetics
absorbed: rapidly and orally
distributed: onset 30 min, peak 1-2 hrs, duration 4 hrs
metabolized : liver
exreted: kidneys
135
acetompinophen side effects
rash uticaria, nausea, fever, neutropenia, thrombocytopenia, jaundice, hepatotoxicity, hepatic necrosis
all Rare
136
acetompinophen interaction
caution w/ hepatic disease/ other drugs that could cause liver damage
may axacerbate anemias
137
acetominophen contradiction
hepatic disease, viral hepatitis, alcoholism
138
acetominophen overdose
glutathione, which converts toxic metabolit into nontoxic, quickly depleted in overdose.
accumulation occurs, equals liver damage
139
S&S acetominophen overdose
anorexia, nausea/vomiting, pallor, abdominal discomfort, jaundice
140
acetominophen antidite
acetylcysteine
