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exam 2 Flashcards

1
Q

T/F

Sedative/hypnotic agents possess good analgesic properties

A

false

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2
Q

chronic pain

A

difficult to identify source
assoc. with a complicated set of behavioral issues
pharm approach is only one comp. of management of chronic pain

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3
Q

acute pain

A
  • tissue injury and inflammation
  • mediated by biochemical mediators: histamine, prostaglandins, bradykinin
  • PGE2 causes hyperalgesia by sensitizing afferent nociceptive receptors to histamine and bradykinin
  • CNS A delta and C fibers of cranial nuclei V, VII, IX, X to nucleus caudalis of medulla and then to higher brain centers
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4
Q

pharmacological management as adjunct to treatment of _______ is appropriate

A

acute pain

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5
Q

Non-narcotic analgesics

A
  • salicylates (aspirin)
  • acetaminophen
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
  • COX 2 inhibitors
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6
Q

examples of NSAIDs

A
  • ibuprofen
  • naproxen
  • naproxen sodium
  • diflunsial
  • flurbiprofen
  • ketorolac
  • etodolac
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7
Q

ibuprofen

A 
best in dentistry
Non-selective NSAID
adverse GI effects
COX inhibitor ( 1--regulates homeostasis; 2--inducable
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8
Q

COX 2 inhibitors

A

celebcoxib
Rofecoxib (withdrawn)
better for GI tract
selective

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9
Q

what do corticosteroids inhibit?

A

Phospholipase A 2

antiinflammatory

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10
Q

what does aspirin & NSAID inhibit?

A

cyclooxygenase (non-selective)

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11
Q

PGI2

A

prostacyclin (endothelium)

- vasodilation; decreased platelet aggregation

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12
Q

PGE2/PGF2e

A 
prostaglandin
smooth muscles
vasodilation, edema
- sensitizes free nerve endings
- mediates pain and inflammation
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13
Q

TXA2

A

thrombozanes
platelets
vasoconstriction; increased platelet aggregation

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14
Q

aspirin made of

A

salicylic acid, sodium salicylate, acetylsalicylic acid

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15
Q

antipyretic action of apsirin

A

occurs centrally (ibhibition of PGE2)
effective in febrile pts
little effect on normal body temp
IL1 (endogenous pyrogen) triggers synthesis of CNS Prostaglandins

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16
Q

analgesic action of aspirin

A

mediated thru central and peripheral mechanisms:

  • salicylates inhibit synthesis of prostaglandins in inflamed tissues–> prevent sensitization of pain receptors
  • analgesic site close to antipyretic region in hypothalamus (doesn’t cause sedation)
  • max effect–> 650-1000 mg
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17
Q

antiinflammatory effects of aspirin

A

inhibition of PG synthesis

also inhibition of leukocyte phagocytosis, suppression of immulogical process and stabilization of lysosomal membranes

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18
Q

hematologic effects of aspirin

A
  • products of PG path (thromboxane A2, prostacycline, ,PGI2) have major influence on initiation and inhibition of platelet aggregration
  • platelet agg. related to clot formation and bleeding time
  • aspirin decreases platelet aggregation (more bleeding)
  • **effect of aspirin on platelets due to irreversible inhibition (acetylation) of enzyme cyclooxygenase
  • inhibition of platelet TXA2 synthesis –> over activity of vascular PGI2
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19
Q

at high doses, aspirin decreases ______and impairs _____

A

decreases plasma prothrombin and impairs coagulation

sodium salicylate has much less effect on prolonging bleeding time

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20
Q

maximum dose of aspirin’s effect on respiratory system

A
  • partial uncoupling of oxidative phosphorylation
  • increased CO2 production
  • compensatory increase in ventilation prevents changes in plasma pH
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21
Q

toxic dose of aspirin effect on resp system

A

stimuates ventilation by effects on receptors in medulla

  • –> respiratory alkalosis (due to increased CO2)
  • compensated by renal elimination of bicarbonate, sodium, and potassium
  • reduction in bicarbonate impairs bicarbonate buffering capacity
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22
Q

therapeutic dose of aspirin on resp system

A

minimal effect

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23
Q

what happens as aspirin doing increases?

A

metabolic acidosis due to uncoupling of oxidative phosphorlyation

  • other factors that contribute: acidity depression of resp center, loss of bicarbonate buffering capacity, changes in carb met
  • *fatal metabolic/respiratory acidosis and respiratory paralysis
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24
Q

effects of aspirin on cardio system

A

little effect at therapeutic doses

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25
Q

GI effect of aspirin

A

GI distress
occult bleeding
sudden acute hemorrhage

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26
Q

effect on kidney from aspirin

A

analgesic nephropathy (loss of prostaglandins that regulate bloodflow)

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27
Q

effect on liver from aspirin

A

subclinical hepatoxicity

no overt changes

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28
Q

diflunsial

A

salicylate that can be taken twice daily

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29
Q

pharmokinetics of aspirin

A
  • absorption from stomach and small intestine
  • rate limiting step: disintegration/dissolution
  • hepatic metabolism (glycine and glucuronide conjugates)
  • weak acid
  • renal elimination
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30
Q

therapeutic uses of aspirin

A
  • analgesic, antiinflammatory, antipyretic
  • dose: 650-1000 mg
  • all painful conditions
  • not rec for gout
  • low dose for reducing cardio incidents
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31
Q

therapeutic uses of aspirin in dentistry

A

equal or greater pain relief than codeine (narcotic)

- ceiling effect in pain relief (will end up with more adverse effect)

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32
Q

adverse effects of aspirin

A

nausea, GI irritation, occult GI bleeding, increase in bleeding time

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33
Q

chronic toxicity of aspirin

A

“salicylism”

tinnitis, nausea, headache, hyperventilation, menal confusion

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34
Q

acute toxicity of aspirin

A
  • cardinal signs: tinnitis, hyperthermia, hyperventilation
  • followed by combined resp and metabolic acidosis accompanied with dehydration
  • acidosis is more common as level of overdose increases
  • impaired vision, hallucination, delirium
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35
Q

treatment of aspirin overdose

A
  • palliative and supportive
  • resp support
  • gastric lavage
  • maintenance of electrolyte balance
  • maintenance of plasma pH
  • alkalization of urine by bicarbonate
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36
Q

why can some people not tolerate aspirin?

A
  • range from rhinitis to severe aspirin
    -bc of:
  • loss of production of bronchodilator PGE 2
  • lipooxygenase pathway predominates (SRSA pathway)
  • intolerance also shown by: urticaria (hives) and angioedema
  • cannot switch to NSAIDS
    (alternative–> acetometophin)
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37
Q

contraindications to use of aspirin

A

ulcer, asthma, diabetes, gout, flu, varicella, hypocoagulation

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38
Q

adverse effects of aspirin with flu, varicella

A

reye’s syndrome in children

recent viral infection–> use acetometophin instead

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39
Q

warfarin + aspirin

A

internal bleeding, poss hemorrhaging

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40
Q

heparin + aspirin

A

internal bleeding, poss hemorrhaging

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41
Q

probenecid, sulfinpyrazone + aspirin

A

decreased urocosuric effect, reappearance of gout (drugs should be treatment of gout)

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42
Q

chemical name of acetaminophen

A

n-acetyl-p-aminophenol; APAP

(phenacetin & acetanilid –> APAP

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43
Q

acetaminophen has effective analgesic and antipyretic agent but has little _____

A

antiinflammatory activity
(inhibitor of PG synthesis centrally but less effective at inhibition peripherally)
- interaction of APAP with peroxide (present in inflamed tissues) that may reduce APAP effectiveness

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44
Q

at therapeutic dose, acetaminophen has little effect on _____

A

cv/respir systems
no effect on platelet aggregation
no GI bleeding
no gastric irritation or effect on uric acid excretion

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45
Q

pharmacokinetics of acetaminophen

A
  • well absorbed from small intestine
  • well distributed to tissues and crosses placenta
  • hepatic metabolism (glucuronide conjugation)
  • renal elimination via both GFR and tubular secretion
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46
Q

general therapeutic uses of acetaminophen

A
  • pts for whom aspirin/NSAIDs are contraindicated

- 650-1000 mg dose

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47
Q

adverse effects of acetaminophen

A

-major metabolite of this drug cause **hepatotoxicity (toxic doses range >4 /day )–> depletion of glutathione and subsequent alkylation of liver proteins causing cellular injury

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48
Q

tx of acetaminophen overdose

A

gastric lavage

n-acetylcysteine (reducing agent) (must be given during initial 36 hours)

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49
Q

rec dose of acetaminophen

A

325-600 mg and max daily dose less than 3 g

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50
Q

analgesic, antipyretic, and anti-inflamm effects of NSAIDs due to?

A
  • inhibition of PG pathway at level of cyclooxygenase
  • inhibition of PG results in reduction of inflammation and pain
  • ceiling effects exist
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51
Q

major side effects of NSAIDs

A

erosive and ulcerative lesions in the stomach
possible nephrotoxicity
-cross-hypersensitivity reactions have been reported between NSAID’s and aspirin

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52
Q

_______ is an effective treatment of post op pain and inflammation. It is a weak organic acid, highly protein bound (99%) and undergoes extensive hepatic metabolism. Conjugates are excreted in urine.

A

ibuprofen

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53
Q

dosage of ibuprofen

A

400-600 mg q4-6 hrs

max daily dose of 3200mg

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54
Q

naproxen

A
  • free acid or sodium salt (aleve)
  • similar to ibuprofen
  • highly protein bound
  • doesn’t interact with oral anticoagulants and hypoglycemic agents
  • eliminated from kidney
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55
Q

dosage of naproxen

A

220-440 mg naproxen sodium q4-6 h

max daily dose 660 mg

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56
Q

______ is formulated for oral and parentral routes of admin. Has potential of renal toxicity if taken for more than 5 days. It has antiplatelet activity and is contraindicated before surgery

A

ketorolac

also comes in nasl spray

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57
Q

diflunisal

A
  • derivative of salicylic acid
  • not met. into salicylate
  • extended duration of action
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58
Q

dosing of diflunisal

A

loading dose of 1000 mg followed by 500 mg q8-12 hr

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59
Q

adverse effects of NSAIDs

A
  • gastric irritation (with long term use; ulcers in 6% of pts; 100,000 hospital admissions and 16,000 death/year)
  • fluid retention
  • nephrotoxicity
  • transient and reversible inhibition of platelet aggregreation
  • dizziness
  • clinical signs of OD similar to salicylates
  • contraindications: similar to aspirin
  • risk of kidney injury in fetus if taken while preg
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60
Q

examples of selective COX2 inhibitors

A
  • rofecoxib and valdecoxib (removed from market)
  • celecoxib
  • etoricoxib
  • etodolac
  • melxicam
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61
Q

selective COX2 inhibitors

A
  • 8-35X more selective for COX2 isozyme
  • 50-60% reduction in adverse GI effects; adverse renal effects can still occur
  • increased CV events
  • potentially life threatening asthmatic or allergic reactions in aspirin intolerant individuals
  • allergy to sulfonamides should avoid use of celecoxib
  • interact with warfarin to increase risk of bleeding
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62
Q

opium poppy made of:

A
  • 5-20% morphine
  • 0.5-2.5% codeine
  • papaverin (smooth muscle relaxant)
  • other alkaloids
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63
Q

opiates

A

alkaloids that are derived or isolated from opium

ex: morphine (greek god of sleep)

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64
Q

opioids

A

substances that are not derived from opium and do not have morphine-like structures, but do have morphine-like pharmacological properties
- whole group known as opioids analgesics

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65
Q

narcotic analgesics

A

compounds that produce analgesia, drowsiness, and dreamy detached feeling (euphoria)

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66
Q

endogenous opioids

A

enkephalins, endorphins, dynorphins

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67
Q

narcotic agonists

A
  • naturally occurring substances (opiates): opium, morphine, codeine
  • semisynthetic derivatives (opioids): heronin (acetylmorphine), hydromorphone (dilaudid), hydrocodone, and oxycodone
  • synthetic derivatives (opioids): meperidine (demerol), fentanyl, sufentanyl (fent and suf used in IV general anesthesia)
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68
Q

narcotic agonist/antagonists

A

pentazocine (talwin)

nalbuphane (nubain

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69
Q

narcotic antagonists

A
  • naloxone (narcan)

- naltrexone (trexan)

70
Q

effects of opioids

A 
analgesia
respiratory depression
constipation
GI spasm
dependence
71
Q

endogenous opioid peptides ranked in order of size

A

endorphins&raquo_space;dynorphins>enkephalins

72
Q

opioid receptors are linked to—

A

g proteins

73
Q

how many membrane spanning alpha helical segments are there for opioid receptors?

A

7

74
Q

mu receptors

A

principle mediator of opioid analgesia (morphine)

mu1: supraspinal analgesia (above spinal cord)
mu2: spinal analgesia; respiratory depressant & GI actions

75
Q

delta receptors (2 subtypes)

A
  • endogenous ligand: -enkephalins

- produce both spinal and supraspinal analgesia: opioid reinforcement

76
Q

kappa receptors (3 subtypes)

A
  • endogenous ligand: dynorphins
  • spinal analgesia: kappa 1 and 2
  • supraspinal analgesia: kappa 3
  • also dysphoric effects
77
Q

sigma receptors

A
  • mediating/may be involved in antianalgesic effect observed with dextroisomers of certain opioids
  • dysphoric effects of opioids and phencyclidines (PCP–receptor may be inhibit. comp. of NMDA receptor complex which regulates opioid tolerance and dependence
78
Q

where do enkephalins primarily act?

A

in local circuits or CNS interneurons

inhibitory effects

79
Q

what is an important site to morphine analgesia?

A

periaqueductal gray

80
Q

______ opioids modulate the secretion of pituitary gonadotropin from the pituitary

A

endogenous

naloxon causes increases in LH and FSH secretion

81
Q

where does analgesia of opioids take place?

A

central and peripheral mechanisms

PAG

82
Q

pathway of opioids

A

descending pathway – indirect (synaptic relay in medulla)

83
Q

_____ and _____ are the neurotransmitters that ultimately inhibit pain transmission

A

5HT (serotonin) and NE

84
Q

opioids do not affect the response threshold to painful stimuli but the ______

A

interpretation and emotional reaction to stimulus

85
Q

mechanism of action of opioids relate to:

A
  • increase in potassium conductance (relative hyperpolarization and decrease neuronal activity); post-synaptic
  • decrease in calcium influx thru vol. dep. channels (decrease NT release); presynaptic
86
Q

net effects of opioids

A

general inhibitory acute effects mediated by effects of opioids on ion channels of neurons

87
Q

Pharm effect of opioids on CNS

A 
analgesia
drowsiness
euphoria/dysphoria
resp depression
decrease cough reflex
pupillary constriction
decrease secretion of LH and FSH
increase prolactin secretion
stimulation of medullary CTZ (enhanced emesis followed by depression of vomiting rxn)
88
Q

pharm effect of analgesia of opioids

A
  • dose dependent pain relief which is selective (vision and hearing unaffected by therapeutic doses
    10 mg parenteral or 30 mg oral/ 70 mg morphine
  • no ceiling effect
  • sites: peripheral, central (spinal/supraspinal)
  • usually parenterally given
89
Q

emergency measure for chest pain

A

10 mg morphine

90
Q

what kind of pain are opioids best at controlling?

A

dull, aching pain

-neuropathic pain less responsive to opioids

91
Q

aging does what to pain?

A
  • decreases sensitivity to pain
  • reduces ability to clear morphine (increases elimination 1/2 life)
  • morphine-induced pain relief increases with age in elderly
92
Q

effects of opioids on resp. system

A
  • dose-dependent
  • decreases in tidal volume and rate
  • decreases response of brainstem resp center to CO2 tension in blood
  • suppresses pontine/medullary centers that regulate respiratory frequency
  • all opioids suppress respiration
93
Q

chest wall rigidity

A
  • seen with IV opioids (e.g. fentanyl)
  • increase in muscle tone
  • —> truncal stiffness
  • more prevalent with bolus administration, in elderly patients and those receiving N2O:O2
  • can be treated with naloxone or a neuromuscular blocker
94
Q

cough suppression with opioids

A
  • antitussive effect by depression neuronal activities in brainstem
  • codeine, dextrometorphan
  • suppression occurs at dosages lower than analgesic or respiratory doses
95
Q

pupillary constriction

A
  • morphine causes miosis in humans
  • mediated by oculomotor nerve
  • tolerance does not develop
96
Q

why nausea/vomiting with opioids

A
  • stimulate CTZ in medulla –> vomit (emesis)
  • initial stimualtion followed by depression of brainstem medullary center
  • vestibular component freq seen in ambulatory rather than recumbent patients
97
Q

effect of opioids on GI tract

A

constipation

increase smooth muscle tone and decrease propulsive motility throughout GI tract (stomach/duodenum transit delay)

98
Q

treatment of diarrhea

A

diphenoxylate + atropine

  • biliary smooth muscle spasm (painful)
  • inhibition of intestinal hypersecretion (treats diarrhea), gastric acid, pancreatic, biliary, intestinal secretion
99
Q

opioid effect on smooth muscle cells

A
  • increase tone of smooth muscles of ureter, urinary bladder, uterus, and bronchioles (minimal effect at therapeutic dose)
  • decrease urine flow
  • antidiuretic effect of opioids
  • increases tone of uterus but labor duration not affected
  • may aggravate asthmatic attack–> histamine release
  • may lead to : stop urine flow, increased uterine tone during labor, increase neonatal morbidity, bronchoconstriction at HIGH doses
100
Q

effects of opioids on cardiovascular system

A
  • toxication decreases BP bc of resp depression and hypoxia
  • release of histamine–> vasodilation (more for morphine than fentanyl)
  • decrease peripheral vascular response –> orthostatic hypotension
  • cerebral vasodilation : may relate to morphine-induced decreased respiration causing increases in blood CO2
101
Q

why is morphine helpful in pulmonary edema?

A

peripheral pooling of blood

102
Q

acute opioid toxicity

A
  • death bc of resp depression
  • cardinal signs: stupor, constricted pupils, decreased respiration
  • as severity of intoxication increases –> coma, decrease in BP if hypoxia is not altered
103
Q

management of acute opioid toxicity

A
  • support of respiration; patient airway
  • dilation of pupils and shock: both caused by persistent hypoxia
  • administer naloxone: short duration of action: continuous monitoring
  • naloxone admin to opioid-dep pt —> withdrawal symptoms
104
Q

opioid tolerance signs

A
  • tolerance develops to depressant (anal, drowsiness, and resp depression) but NOT to stimulant effects (pup constriction and constipation)
  • tolerance develops to euphoria
  • the greater the opioid dose and shorter the interval between doses, the more rapid the development of tolerance
105
Q

signs of dependence on opioids

A
  • only apparent in absence of drugs
  • physical vs psych dep
  • dose related
  • greater dose and longer duration, greater dep
  • blockade of NMDA receptors and NO synthase prevent tolerance and dependence without reducing analgesic effects of morphine
106
Q

physical dependence can occur in absence of _____ dependence

A 
psychological dependence (chronic tx of cancer pain)
-tolerance, physical dependence, psych dependence are reversible
107
Q

S & S of opioid withdrawal

A

anxiety and drug craving
anxiety, insomnia, GI disturb, runny nose, mydriasis, diaphoresis
tachycardia, nausea vomiting, hypertension, diarrhea, fever, chills, tremors, seizure, muscle spasms

108
Q

feel normal after ____ days of opioid cessation

A

7-10 days

109
Q

opioids withdrawal symptoms managed with slow taper of either ____ or partial agonist _____ with or without an alpha 2 adrenergic agonist

A

-methadone or buprenophine

110
Q

treatment of choice for most opioid patients

A

buprenorphine with or without naloxone

111
Q

when should methadone be used?

A

when buprenorphine is unavailable or ineffective or in patients who would benefit from daily supervised dosing

112
Q

clonidine and lofexidine

A

alpha2 adrenergic agonists
less effective than methadone or buprenorphine
useful as adjunct to opioid agonist and in settings where use of an opioid agonist is prohibited

113
Q

what works better for morphine–oral or parenteral?

A

oral does NOT work as well

114
Q

pharmocokinetics of morphine

A
  • good parenterally
  • hepatic first pass effect: morphine&raquo_space;codeine
  • morphine –morphine-6-glucoronide (acts on mu receptors and exerts potent analgesic effect)
  • conjugated morphine excreted via kidney; small amount in urine
  • morphine does not accumulate in tissues
  • oral dose 10-2500 mg/24 hrs (cancer–200mg/day): dose titrated, tolerance present, controlled release tabs or caps produce longer lasting analgesia
115
Q

breakthrough pain treated with

A

fentanyl lollipop

116
Q

general therapeutic uses of morphine

A

analgesia
tx of pulmonary edema
inducing sleep for pain or cough

117
Q

general uses for codeine

A 
OCH3 sub for OH at C3 increase oral effect
analgesic, antitussive
10% met into morphine
resp depressant, sedation
10 mg morphine=120 mg codeine
increased nausea or vomiting
slower dev of tolerance 
little physical dep at therapeutic dose
118
Q

antitussive dose of codeine

A

15-20 mg

119
Q

analgesic dose of codeine

A

30-60 mg po

120
Q

codeine

A 
opioid agonist
post operative analgesic
low first pass effect (useful po : 60% bioavail)
onset of action -- 30-45 min
about 10-20% converted to morphine
remaining drug is antitussive
121
Q

hydrocodone and oxycodone

A

opioid agonists

  • derivatives of codeine
  • converted to hydromorphone (dilaudid) and oxymorphone (numorphan) (10-20% conversion)
  • good oral bioavailability
  • alternatives to codeine
  • pharm effects similar to codeine
  • hydrocodone is schedule II substance
122
Q

opioids listed by relative strength (strongest first)

A

morphine and oxycodone
hydrocodone
codeine

123
Q

meperidine

A
  • atropine-like activity –> less pupillary constrict or biliary spasm
  • similar to morphine: analgesic, sedation, resp depress
  • oral effect 1/5 of parenteral effect
  • shorter duration than morphine
  • acute intoxication –> cns excite
  • can & will cause dependence
  • poor CV stability with IV sedation ; fentanyl replaced it
  • contraindicated in pts taking MAOI or amphetamine or with asthma (histamine release)
124
Q

serotonin syndrome

A
  • meperidine inhibits 5Ht reuptake
  • when combined with SSRIs and other antidepressants
  • mild version : shivering and diarrhea
  • severe: CNS manifest—tremors and seizure
125
Q

methadone

A
  • equipotent to morphine
  • better oral efficacy than morphine; otherwise differs little
  • analgesia, sedation, resp depress, miosis, antitussive, subjective effects similar to morph
  • replacement for heroin addicts
    - oral efficacy
    - persistent effect when repeated
    • single daily dose –less withdrawal
    • less intense withdrawal S & S
  • treatment of opioid depend related to cross tolerance and cross-dependence
126
Q

cross dependence

A

if pt is dependent on one opioid, they can be switched to another opioid to suppress S & S of withdrawal

127
Q

alternatives to methadone

A

levomethadyl (ORLAM)

dose: q3d bc long duration of action

128
Q

propxyphene

A

type of methadone
analgesic
subject to abuse, physical dependence during high dose, long-term use
-less dependence than codeine

129
Q

fentanyl and congeners (fentanyl like things)

A
  • potent analgesics with relatively short duration of action
  • IV supplements during general anesthesia with inhalation
  • more lipid soluble than morphine
    • meperidine: poor CV stability
    • more rapid onset of action and short duration of action (80-100X more potent than morph)
130
Q

advantages of fentanyl

A

provide cardiovascular stability and reduce endocrine and metabolic responses during surgery

131
Q

what drug replaced meperadine and why?

A

fentanyl

because meperidine has a poor CV stability

132
Q

neurolepanlgesia

A

sedated analgesia

fentanyl + droperidol (INNOVAR)

133
Q

examples of mixed-acting agonist-antagonist

A
  • pentazocine
  • butorphenol
  • buprenorphine
  • nalbuphine
134
Q

what is an agonist at the kappa and partial agonist or weak antagonist at mu receptors?

A

pentazocine

135
Q

what was developed as effect to produce agonist without abuse potential or dependability?

A

pentazocine (still abused)

136
Q

what preparation was made to prevent abuse of pentazocine?

A

mixture of pentazocine and naloxone (Talwin NX)

  • Naloxone has little effect po
  • therefore preparation is still good po but without effect parenterally
137
Q

why can’t pentazocine be used as a substitute for morphine?

A

does not antagonize resp depressant property of morphine or suppress withdrawal symptoms in individuals dependent on other opioids

138
Q

pentazocine can cause an abstinence syndrome bc of ______

A

residual antagonist effect at mu receptors

139
Q

what is the metabolism of pentazocine?

A

well absorbed po–> liver metabolism–> glucuronide conjugate–> urine

140
Q

how potent is pentazocine compared to morphine?

A

1/3 as potent parenterally (I.m.)

141
Q

adverse effects of pentazocine

A

-n/v and sedation (similar to other opioids)

142
Q

whats different about pentazocine compared to other opioids ?

A

can increase both heart rate and blood pressure

143
Q

toxic doses of pentazocine cause—

A

dysphoria (kappa receptor effect)

respiratory depression but does not increase with increasing dose as it does for opioid agonists

144
Q

buprenorphine

A
  • multi-mechanistic–partial agonist of mu receptor, partial antagonist of kappa receptor and some nonopiod receptor activity
  • agonist effects qualitatively similar to morphine
  • produces less respiratory depression than morphine at same dose; may be more difficult to reverse using naloxone
  • causes less euphoria than many other opioids
  • *useful in chronic addiction control
145
Q

naloxone

A
  • short acting
  • iv admin
  • antidote for resp depression secondary to opioid overdose
  • rapidly improves ventilation; additional doses may be required
  • additional doses may be required to antagonize long-acting opioid agonists
146
Q

naltrexone

A
  • long acting
  • oral admin
  • maintenance of detoxified opioid abusers
  • single dose can suppress the effect of opioid agonist 48-72 hrs
  • tx of morphine overdose – monitor pt in case of resp depression relapse
147
Q

tramadol (ultram)

A
  • weak mu receptor agonists (metabolite is more potent)
  • inhibits reuptake of NE and 5HT
  • analgesic effect partially reversed by naloxone
  • perioperative agent–relieves mod-severe pain
148
Q

most common adverse effects of tramadol

A

n/v
drowsiness
minimal resp and CV issues

149
Q

_____ have been reported for tramadol

A

seizures

150
Q

admin of tramadol

A

oral and terminal half life is 7 hrs

151
Q

dosage of tramadol

A

50-100 mg q4-6 po
don’t exceed 400 mg/day
severe pain — 100 mg initial dose

152
Q

tramadol is what level substance?

A

schedule IV

153
Q

ultrased

A

combo of tramadol with APAP

154
Q

tapentadol (nucynta)

A
  • opioid agonist
  • inhibits norepinephrine reuptake; schedule II
  • lower incidence of adverse effect than opioids
  • inferior analgesic effect in acute postsurg dental pain
  • **may cause serious, life-threatening, breathing problems initially or after dose increase
  • add on agent for breakthrough pain with NSAID or APAP
155
Q

when do you prescribe Rx NSAID and opioid?

A

severe pain (codeine, hyrdocodone, oxycodone)

156
Q

Rx NSAID used with

A

moderate pain

157
Q

mild pain–you use–

A

OTC aspirin, aceto, ibu, naproxen

158
Q

pre-emptive measures before surgery

A

NSAID

159
Q

3 and #4

A

aspirin and codeine
325/30 mg
325/60 mg

160
Q

percodan

A

apsirin and oxycodone

325/5

161
Q

tylenol #3

A

acetaminophen and codeine

300/30

162
Q

vicodin
lortab
norco

A

acetaminophen and hydrocodone
325/5
325/7.5
325/10

163
Q

percocet

A

acetaminophen and oxycodone
325/5
325/10

164
Q

ultram

A

tramadol
50
ER: 100, 200, 300

165
Q

ultracet

A

acetaminophen and tramadol

325/37.5

166
Q

vicoprofen

A

ibuprofen and hydrocodone

200/7.5

167
Q

combunox

A

ibuprofen and oxycodone

400/5

168
Q

1 grain of tylenol =

A

60 mg

169
Q

tylenol 4 is how many grains

A

full grain

170
Q

tylenol 3 is how many grains

A

1/2 grain

171
Q

national drug overdose deaths for opioids

A

17,029

172
Q

______ are leading contributer to epidemic drug abuse. Safe and informed prescribing practices and sensible guidelines can stop it.

A

safe prescribing practices

neuro 2 (3 decks)

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