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3rd Quarter > Pharm Quiz 2 > Flashcards

Pharm Quiz 2 Flashcards

0
Q

What are 3 Phenylpiperidine derivaties of synthetic opioids?

A
  1. fentanyl
  2. Sufentanil
  3. remifentanil
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1
Q

What receptors sites do opioid antagonist/agonist interact with?

A

Mu
Kappa
Delta

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2
Q

Phenylpiperdines vary greatly in _____ & _____ between _____ & _____ _____ _____.

A

potency & equilibration
plasma & site of action

(ex. demerol to carfentanil)

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3
Q

What types of receptors and where are they located that opioids primarily act upon?

A

sterospecific receptors at pre and post synaptic sites in the CNS(brainstem & spinal cord)

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4
Q

Opioid receptors are designed to be activated by endogenous opioids. What are these endogenous opioids?

A
  1. Endorphins
  2. Enkephalins
  3. Dynorphins
  4. Endomorphins
  5. Nociceptin
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5
Q

Only ____ & ____ forms of opioids bind to receptors. Opioid receptor activation decreases neurotransmission via _____ _____ _____.

A

nonionized & levorotary

presynaptic neurotransmitter inhibition

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6
Q

What was the first drug shown to bind to mu receptors?

A

Morphine

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7
Q

What was the first drug found to bind to kappa receptors?

A

Ketocyclazocine-no longer in use.

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8
Q

What are two drugs used today that interact with kappa receptors?

A

nubain and staidol

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9
Q

4 characteristics of kappa receptors?

A
  1. activated by endogenous opioid dynorphin
  2. there is a ceiling affect, usually not potent enough to stop surgical pain
  3. mixed agonist/antagonist sites
  4. mediates analgesia less than mu receptors(mediate dysphoria, sedation)
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10
Q

What endogenous opioid receptor do Delta interact with and what do they facilitate?

A

enkephalin and facilitates mu activities

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11
Q

What endogenous opioid receptor do Nociceptin receptors interact with and how does is affect mu agonist?

A

Endogenous opioid nociceptioin
develops tolerance to mu agonist
instinctive and emotional behaviors

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12
Q

What is the opioid receptor function?

A

endogenous pain suppression system

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13
Q

What are the 5 receptor location for opioids?

A

periaqueductal gray matter in:

  1. brainstem
  2. amygdala
  3. corpus striatum
  4. hypothalamus
  5. substantia gelatinosa of the spinal cord
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14
Q

Opioid receptors are involved in(3)?

A
  1. pain perception
  2. integration of pain impulses
  3. pain response
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15
Q

What are neuroaxial opioids?

A

opioids that are delivered into the epidural or subarachnoid tracts

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16
Q

How do neuroaxial opioids provide analgesia?

A

effect due to mu receptors in SUBSTANTIA GELATINOSA OF THE SPINAL CORD

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17
Q

How much more is the epidural opioid dose more then the subarachnoid dose?

A

5-10 times more

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18
Q

Epidural opioid placement works via (2)?

A
  1. mu spinal cord receptors

2. systemic action

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19
Q

Epidural fentanyl/sufentanil works in part via SYSTEMIC absorbition….what is it dependent upon?

A

how lipid soluble it is

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20
Q

The absorbtion of epidural does of opioids is dependent upon what 3 things?

A
  1. epidural fat
  2. systemic absorption-epidural space venous plexus
  3. CSF
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21
Q

Cephalad movement of opioids is dependent upon what two thing?

A
  1. greater with less lipid soluble opioids like morphine

2. follows CSF currents into cisterna magna > fourth and lateral ventricles

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22
Q

What are 2 reasons for adverse effects of neuroaxial opioids?

A
  1. greater CSF concentrations

2. greater systemic concentrations

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23
Q

List 8 adverse effects of neuroaxial opioids.

A
  1. pruitis
  2. N&V
  3. urinary retention
  4. respiratory depression(lethal adverse effect)
  5. sedation
  6. constipation
  7. poikothermia
  8. water retention(ADH secretion)
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24
Q

What are the 4 main side effects of neuroaxial opioids.

A
  1. pruritis
  2. urinary retention
  3. ventilatory depression
  4. sedation

Side effects are dose dependent

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25
Q

What is the number 1 side effect of neuroaxial opioids?

A

PRURITIS-especially face, neck and upper thorax

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26
Q

What causes the side effect of pruitis with neuroaxial opioids?

A

Not from histamine but cephalad migration in CSF to trigeminal nucleus

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27
Q

What is the treatment for neuroaxial opioid puritis?

A

naloxone(#1), antihistamines

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28
Q

What are some characteristics of the Neuroaxial opioid side effect of urinary retention?

A
  1. most common in young males
  2. Neruoaxial urinary retention more common than IM/IV
  3. Due to opioid receptor activation in sacral spinal cord
  4. inhibits sacral parasympathetic outflow causing: detrusor muscle relaxation & greater bladder capacity
  5. may be reversed by naloxone
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29
Q

What is the most serious adverse effect of neuroaxial opioids? What is the mechanism of action.

A

VENTILATORY DEPRESSION

1% incident

depression within 2 hours due to systemic absorption(not cephalad migration)

depression after 2 hours due to cephalad migration of opioids in CSF—> interaction with ventral medulla

occurs most often with morphine

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30
Q

What are the characteristics of Neuroaxial opioid sedation.

A
  • dose related
  • most common with sufentanil because it is the most lipid phillic has the most systemic absorbtion.
  • sedation accompanies ventilatory depression!
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31
Q

Morphine induced CNS excitation is caused by?

A

cephalad migration, interaction with non-opioid receptors

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32
Q

What are 6 other effects neuroaxial opioids can have on the body?

A
  1. delayed gastric emptying
  2. lower body temp(inhibition of shivering)
  3. water retention due to vasopressin release
  4. spinal cord damage(if opioids with perservatives~duromorph~ is used
  5. reactivation of herpes 2-5 days post opioids
  6. newborns with ventilatory depression
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33
Q

Morphine is the prototype _____ opioid _____.

A

mu, agonist

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34
Q

Morphine is effective for _____ & _____ muscle pain

A

visceral and skeletal

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35
Q

When analgesia best achieved with morphine?

A

before pain

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36
Q

Why is PO morphine unreliable?

A

first pass clearance

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37
Q

What are the characteristics of IM morphine?

A
  • well absorbed
  • onset 15-30 minutes
  • peak 45-90 minutes
  • duration 4 hours
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38
Q

What are 3 characteristic of the peak effects of morphine?

A
  1. peak effect delayed compared to fentanyl(slower BBB penetration)-due to being less lipophiliac
  2. CSF {} peaks 15-30 minutes after administration
  3. analgesic and ventilatory effects seen after plasma {} peaks
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39
Q

Why does morphine have poor CNS penetration(4)?

A
  1. high amount of ionization of 7.4 pH
  2. poor lipid solubility
  3. protein binding-longer duration of action if Renal impared
  4. rapid conjugation via glucuronic acid
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40
Q

What amount of morphine reaches CSF?

A

only small amounts (0.1%)

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41
Q

What is the result of morphine having a high accumulation in kidneys, liver and skeletal muscle?

A

large volume of distribution

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42
Q

What is the main metabolic pathway of Morphine?

A

mainly glucuronic acid conjugation in liver & kidney

  • 75-85% changed to morphine-3-glucuronide, pharmacologically INACTIVE
  • 5-10% changed to morphine-6-flucuronide(black tar heroin)-greater analgesia than morphine
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43
Q

How is morphine eliminated?

A

via urine

  • cumulative effects in ESRD patients
  • Glucuronide metabolism impaired with MAO patients(results in exaggerated effects)

Neonates are more sensitive to ventilatory depressant effects of morphine

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44
Q

What are the CV side effects of morphine(5)?

A
  1. reduced venous return(decreased CO, lower BP)
  2. decreased SNS tone to capacitance vessels(vessels that holds the bodies blood volume
  3. bradycardia-greater vagus nerve activity from stimulation of vagal nuclei in medulla
  4. histamine release-may lower BP
  5. treatment with H1&H2 blockers minimizes hypotentioin
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45
Q

How might the hypotensive effects of morphine be marginalized?

A
  • give no faster than 5mg/min
  • supine position
  • give fluids to “fill the tank”
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46
Q

What is the #1 treatment for morphine induced puritis?

A

narcan

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47
Q

Morphine with nitrous will _____ the _____?

A

depress, myocardium

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48
Q

Greater drops in BP seen with _____ administration with _____.

A

cocomitant, benzodiazepines

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49
Q

By what action does morphine cause ventilatory depression?

A

via agonist effect on the brainstem ventilation centers

50
Q

How does morphine effect the respiratory center?(5)

A
  1. Morphine decreases sensitivity of ventilatory centers to CO2
  2. Morphine interferes with pontine and medullary ventilatory centers that regulate breathing rhythm
  3. decreased RR, greater VT-changes in pattern of breathing(net result-increased PaCO2)
  4. Morphine depresses airway ciliary activity
  5. Morphine increases airway resistance(bronchial smooth muscle actions & release of histamine)
51
Q

What counteracts the ventilatory depressive effects of morphine?

A

pain

52
Q

Why is morphine bad for neuro patients specifically?

A
  1. decreased wakefulness bad for neuro exams(sometimes they use remifentanil cause its short acting you can wake the patient up for a neuro exam)
  2. ventilatory depression which raises ICP via increased cerebral blood flow from higher PaCO2
53
Q

By what mechanism does thoracic and abdominal rigidity(lead chest) occur with morphine administration?

A

with rapid administration due to actions on dopaminergic and GABA neurons

54
Q

By what mechanism does miosis occur with morphine?

A

excitation of Edinger-Westphal nucleus of the oculomotor nerve

55
Q

What are some side effects of morphine seen on the biliary/GI systems?

A
  1. spasms of biliary smooth muscle(increased intrabiliary pressures which causes angina like pain-relived by NARCAN, glucagon or NTG)
  2. may constrict smooth muscle of the pancreatic duct raising amylase and lipase levels
  3. constipation-weaker peristalsis, increased sphincter tone, slower passage causes greater water absorption
56
Q

What are some characteristics of morphine administration and N&V?

A
  • result of direct stimulation of the chemoreceptor trigger zone in the floor of the fourth ventricle(dopaminergic agonist at CTZ dopamine receptors)
  • less common when given IV(IM morphine depresses medullary vomiting center simultaneously with CTZ)
  • less common also in supine patients(vestibular component)
57
Q

What are some GU side effects seen with morphine?

A

GU-greater ureteral tone and peristalsis, may be reversed by anticholinergics
Urinary urgency-via augmentation of detrusor muscle tone yet vesicle sphincter muscle tone is increased, making voiding difficult

58
Q

How does morphine affect the cutaneous tissue?

A
  • vasodilation due to histamine release which leads to:
    1. urticaria, erythema
    2. flushing of face, neck, and upper chest–>may make nose itch(flushing where folks normally “blush”)
59
Q

What is the addiction potential of morphine?

A
  • tolerance and physical dependence occurs with repeated use
  • tolerance/addiction are major limitations to use
  • tolerance occurs in less then 2-3 weeks, complete physical dependence in 25 days, some physical dependence in 48 hours
60
Q

What are the S/S of Morphine withdrawal?

A

yawning, diaphoresis, insomnia, restlessness, abdominal cramps, N&V, diarrhea

withdrawals begins in 15-20 hours from last dose, peaks in 2-3 days, last 10-14 days

61
Q

Meperidine(demorol) was the first synthetic opioid derivative and interacts with what 2 pain modulators?

A
  1. Mu

2. Kappa

62
Q

Meperidine is a product of using _____ _____ with dichloroethyl methyl amine.

A

benzyl CYANIDE

63
Q

How does Meperidine compare to morphine?

A
  • 10% the potency of morphine.
  • structurally related to fentanyl
  • shorter duration of action…..2-4 hours.
  • equal to morphine in sedation, euphoria, N&V and ventilatory depression

demorol is fentanyl grandfather

64
Q

What is the principle metabolic of Meperidine?

A

nor-meperidine(1/2 meperidine’s analgesic potency)

65
Q

Is Meperidine well absorbed from the GI system and how much is lost via first pass clearance?

A

Yes it is well absorbed

half lost in first pass clearance

66
Q

When patients say they are allergic to Meperidine they are usually referring to wha 3 side affects produced by its principle metabolite nor-meperidine?

A
  1. CNS stimulation
  2. myoclonus
  3. seizures
67
Q

What is Nor-meperidines 1/2 life?

A

elimination half life 15 hours(longer than demerol)

68
Q

(T/F)Nor-meperidine has been implicated in confusion and hallucinations, especially in long term and PCA meperidine use.

A

True

69
Q

How much of Meperidine is plasma protein bound, which results in greater effects in(3)?

A

60%;

  1. elderly
  2. malnourished
  3. liver failure
70
Q

Meperidine has the _____ therapeutic index of any clinical opioid.

A

Narrowest

(Plasma {} changes as small at 0.05 mcg/ml can represent pain to complete analgesia and ventilatory depression

71
Q

What is the principle use of Meperidine?

A
  • analgesia for labor and delivery
  • post-op pain relief
  • shivering in PACU(Kappa-mediated: change in shivering threshold)
72
Q

If an epidural opioid agonist is less lipophilic, such as morphine, will it exert less of an effect and require a higher dose or more of an effect and a smaller dose?

A

Less of an effect and require a higher dose

73
Q

If you use a more lipophilic epidural opioid agonist such as fentanyl or sufentanil, systemic absorption will play a greater role in exerting pharmacologic effects(T/F)?

A

true

74
Q

What portion of morphine will actually reach the brain?

A

-0.1%
-poor CNS penetration due to :
high amount of ionization at 7.4 pH
poor lipid solubility
significant protein binding
rapid conjugation via glucuronic acid
-high accumulation in kidney, liver and skeletal muscle

75
Q

What are 2 major reasons to not give demerol to a cardiac patient?

A
  1. increase in HR(structurally similar to atropine)

2. myocardial depressant

76
Q

Describe Fentanyl

A
  • Phenylpiperidine derivative r/t meperidine
  • 75-125 x stronger than morphine
  • more rapid onset, shorter duration of action, greater lipid solubility
  • rapid distribution to inactive tissues(fat/skeletal muscle)
  • Lungs: large inactive storage site…takes up to 75% of initial dose
  • much greater volume of distribution than morphine(greater lipid solubility)
77
Q

What is fentanyl metabolized to?

A
  • Nor-fentanyl, which undergoes renal excretion
  • minimal analgesic potency
  • much greater volume of distribution than morphine(greater lipid solubility)
78
Q

Once inactive tissue sites become saturated with repeated doses of fentanyl, it changes from short acting to long acting drug(t/f).

A

true; fentanyl plasma {} sustain content high rate

79
Q

What is the fentanyl dose for analgesia?

A

1-2 mcg/kg

80
Q

What is the fentanyl dose as adjuvant to inhaled anesthesia?

A

2-20 mcg/kg; will blunt circulatory response to laryngoscopy and sudden increases in surgical stimulation

81
Q

When used as sole surgical anesthetic, what is the fentanyl dose and what is its effect?

A
  • 50-150 mcg/kg
  • not reliable amnesia
  • post-op ventilatory depression
  • sympathetic breath through
  • absorbed by CPB circuits
  • NOT a myocardial depressant
  • NO histamine release
  • suppression of stress response
  • IV and transdermal, lollipop
82
Q

How much fentanyl is delivered via a lollipop?

A

5-20 mcg/kg

-increased incidence of PONV and hypoxemia

83
Q

How much fentanyl is delivered with a transdermal patch?

A

75-100 mcg/hr

-peak effects in 18 hours

84
Q

Fentanyl analgesic effects go hand in hand with ventilatory depressant effects(T/F)?

A

true

85
Q

What are the adverse effects of fentanyl?

A
  • persistent/recurrent ventilatory depression

- 2nd plasma peak {} occurs when sequestered fentanyl from gastric fluid/lung washout re-enters systemic circulation

86
Q

What are the CV effects associated with fentanyl?

A
  • minimal dilation of capacitance vessels….by itself(no histamine release)
  • carotid sinus baroreceptor reflex heart control is DEPRESSED
  • bradycardia more prominent than with MS
  • bradycardia dangerous with neonates as stroke volume is fixed(SV+HR=CO)
87
Q

Are there any allergic reactions associated with fentanyl?

A

rare to never

88
Q

What is seizure activity with fentanyl associated with?

A
  • depression of inhibitory neurons

- dose not interfere with monitoring of evoked potentials

89
Q

Fentanyl causes moment increases in ICP even with maintaining baseline ETCO2(T/F)?

A
  • true

- ICP increases joined by decreased cerebral perfusion pressure pressure and lower MAP

90
Q

Describe Sufentanil:

A
  • analogue of fentanyl(sufentanil comes from fentanyl)
  • 5-10 x greater potency
  • less risk of seizures than fentanyl
  • elimination 1/2 time intermediate between fentanyl and alfentanil
  • prolonged elimination in elderly, obese
  • rapid penetration of BBB unlike MS
  • rapidly redestruibution to inactive tissue in small doses
  • cumulative effect in large doses like fentanyl
  • 60% 1st pass pulmonary uptake
  • 92% plasma protein binding = small Vd
  • Alpha-1 acid glycoprotein(#1 plasma protein it binds to)
  • enhanced neonate effect from lower plasma protein levels
91
Q

How is sufentanil metabolized?

A
  • dealkylation into inactive metabolites and

- Demethylation to desmethyl sufentanil

92
Q

Desmethyl sufentanil is 10% as potent as sufentanil(T/F)?

A

true

93
Q

Sufentanil undergoes extensive hepatic extraction…sufentanil clearance sensitive to hepatic blood flow, not to changes in hepatic drug metabolizing capacity(T/F)?

A

true

94
Q

If sufentanil is excreted in urine and stool, what will the effects be for ESRD patients?

A

prolonged ventilatory depression

95
Q

Cessation of sufentanil’s effect is due to _____ and _____?

A

metabolism & redistribution to inactive tissues

96
Q

Single doses of sufentanil produce greater analgesia and less ventilatory depression than fentanyl(T/F)?

A

true; quicker on and quicker off then fentanyl

97
Q

What is the induction dose of sufentanil? Are there any hemodynamic changes?

A
  • 10-30 mcg/kg

- MINIMAL HEMODYNAMIC CHANGES….VERY STABLE

98
Q

Sufentanil bradycardia may be slow enough to decrease CO?

A

true

99
Q

Sufentanil is THE BEST phenylpiperidine derivative for blunting BP and catecholamine responses to surgical pain.

A

True

100
Q

How is Remifentanil different from fentanyl?

A
  • has an ester linkage

- makes it RELATED to fentanyl family

101
Q

Remifentanil is the only IV form of opioid agonist that you can adjust like a vaporizer

A

True

102
Q

What does the unique metabolism of remifentanil provide?

A
  • short action
  • precise titration
  • no cumulative effect
  • rapid recovery
103
Q

How is remifentanil metabolized?

A
  • rapidly metabolized by hydrolysis of propanoic acid-methyl ester linkage by non-specific tissue and blood esterase’s
  • No liver/kidney involvement
  • Patients with atypical plasma cholinesterase metabolize remifentanil normally
104
Q

Remifentanil has a small Vd and rapid clearance. Infusion steady state reached in 10 minutes.

A

true

105
Q

Remifentanil metabolites are pharmacologically inactive.

A

true

106
Q

Name 2 surgeries were remifentanil would be great in?

A
  1. Neuro: for rapid wake-up

2. Retrobulbar block

107
Q

What is the dose for remifentanil?

A
  • 1mcg/kg bolus

- 0.05-2 mcg/kg/min

108
Q

Describe remifentanil>

A
  • Mu receptor agonist
  • comes in a white lyophilized powder…for IV administration after reconstitution and DILUTION!
  • Mu receptor agonist with rapid onset and peak effects, short duration of action
  • No histamine release
  • Synergistic with hypnotics, inhaled anesthetics and benzos
  • effects increase with increasing age of patient
  • does not alter ICP with controlled ventilation maintain ETCO2 less than 30 mmHg
109
Q

For remifentanil blood {} decrease 50% in 3-6 minutes following a 1 min infusion?

A

true

-recovery is rapid; 5-10 min independent of duration of infusion

110
Q

If you adjust your remi gatt, how long will it take to get to steady state {}?

A

5-10 minutes

111
Q

List ways to decrease hypotensive effects of remifentanil.

A
  • lowering infusion rates
  • decrease volatile agents
  • use fluids/vasopressors
112
Q

The duration of remifentanil depression does not increase with the length of infusion, due to a lack of drug accumulation?

A

True

113
Q

What increases risk of “lead” chest?

A
  • single doses(high dose)
  • > 1mcg/kg administered over 30-60 sec
  • infusion rates > 0.1 mcg/kg/min

hypnotics and neuromuscular blockers will block chest wall rigidity effects

114
Q

Codeine is an effective antitussive @ 15 mg PO doses, minimal 1st pass clearance, maximal analgesia @ 60 mg PO

A

True

115
Q

Why is codeine not given IV?

A

histamine release

116
Q

Hydromorphone is a semi-synthetic 8 x more potent than morphine, slightly shorter duration, uses and side effects like morphine.

A

true

117
Q

Methadone is a synthetic opioid effective by oral route, prolonged duration of action useful in chronic pain and suppression of withdrawal and cravings for heroin addicts.

A
  • true

- come from thebane

118
Q

Describe opioid agonist/antagonists

A
  • bind to opioid receptors BUT exert partial effects
  • act on Mu, Kappa and Delta receptors
  • less ventilatory depression
  • limited analgesia(ceiling effect)
  • lower abuse potential
  • may block effects of pure mu agonists
  • Examples: Pentazocine, nubain, stadol
119
Q

What are the adverse effects of opioid agonist/antagonists?

A
  • sedation
  • diaphoresis
  • dizziness
  • dysphoria(minimal with stadol/butorphanol)
  • increased HR
  • increased BP
  • increased LVEDP(not for ASCVD patients)
120
Q

Describe Pentazocine

A
  • opioid agonist/antagonist
  • Benzomorphan derivative
  • delta and kappa receptor action
  • can precipitate opioid withdrawal
  • most often given for pain control in ESRD patients
  • PO, IM, IV routes with extensive 1st pass clearance
  • dose: 10-30 mg IV or 50 mg PO
121
Q

Describe Naloxone

A
  • Alkyl derivative of oxymorphone
  • pure antagonist…no agonist activity
  • displaces opioid agonist from the mu receptor sites and binds to the site without eliciting any response
  • used for opioid induced ventilatory depression, OD, anesthetic misadventures
  • short duration of action may require additional doses for antagonism of prolonged ventilatory depression
  • reverses analgesia
  • increased sympathetic activity after administration > tachycardia, HTN, pulm edema, dysrhythmias
  • administration to opioid dependent moms can trigger withdrawal in neonates as naloxone crosses BBB
122
Q

What is the dose of narcan?

A

1-10 mcg/kg

3rd Quarter (22 decks)

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