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PPNP 3 > Narcotic analgesics (tested), Sedatives & hypnotics (not-tested) > Flashcards

Narcotic analgesics (tested), Sedatives & hypnotics (not-tested) Flashcards

narcotics not added in yet

1
Q

(not tested) Physical symptoms of anxiety

A

(related to adrenergic activation)

Tachycardia
SOB
Nausea
Gastric acid hypersecretion
Trembling

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2
Q

(not tested) Therapeutic rational of anxiety disorders

A

To correct the over-arousal of CNS

Sedative: Causes sedation, relaxation

Hypnotic (one level stronger than sedative): Induces drowsiness and sleep, may have amnestic effects

Anxiolytic: Reduces anxiety

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3
Q

(not tested) What is the main class of drugs used as therapeutics for anxiety disorders?

A

Benzodiazepines

Can be used as anxiolytics/sedatives, hypnotics, pre-anesthetics, or for anti-convulsant effects.

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4
Q

(not tested) Examples of benzodiazepines used as anxiolytics/sedatives

A

Diazepam, lorazepam

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5
Q

(not tested) Examples of benzodiazepines used as hypnotics

A

Diazepam, triazolam, temazepam

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6
Q

(not tested) Examples of benzodiazepines used as pre-anesthetics

A

Diazepam, midazolam

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7
Q

(not tested) Examples of benzodiazepines used for anti-convulsant effects

A

Diazepam

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8
Q

(not tested) Examples of non-benzodiazepines

A

Barbiturates (e.g. phenobarbital)

Buspirone

Zolpidem

Propanolol

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9
Q

(not tested) What is the GABA and GABA receptor? How does it concern us?

A

GABA is the brain’s primary inhibitory neurotransmitter. When GABA binds to its receptors, it reduces the likelihood that a neuron will fire an action potential –> This inhibition is essential for maintaining balancing excitatory and inhibitory signals.

GABA A receptor is the primary target for most sedatives and hypnotics:
- Activation allows chloride to flow into the neuron, hyperpolarizing it and making it less likely to fire.

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10
Q

(not tested) MOA of Benzodiazepines

A

Binds to benzodiazepine site, which in turn potentiates the binding of GABA to the GABA A receptor binding site

Once benzo bound to benzo site, it makes GABA open the chloride channel more easily –> Potentiates influx of chloride ions, leading to hyperpolarization, hence neurons will not be polarised and will not fire –> reduce activation of CNS

Note: Benzodiazepine does not directly bind to GABA binding site!

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11
Q

(not tested) What are some short acting benzodiazepines?

A

Short acting: Short duration of action

Midazolam: Usually used for anxiety, induction of GA, procedural sedation

Triazolam: Used for insomnia

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12
Q

(not tested) What are some long acting benzodiazepines?

A

Usually used for more chronic kind of conditions (e.g. alcohol withdrawal syndrome, status epilepticus, refractory seizure)

Chlordiazepoxide
Diazepam (status epilepticus)

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13
Q

(not tested) What are some intermediate acting benzodiazepines?

A

Usually for anxiety, panic disorders

Lorazepam: Anxiety, insomnia, status epilepticus
Clonazepam: Seizures

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14
Q

(not tested) Which benzodiazepine is used to treat status epilepticus

A

Long acting benzodiazepine.

Diazepam

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15
Q

(not tested) Adverse effects of benzodiazepines

A
  1. Acute toxicity leads to severe respiratory depression
    - especially used with alcohol
    - treatment is by FLUMAZENIL, a benzodiazepine antagonist
  2. Side effects upon chronic use:
    - drowsiness, confusion, amnesia
    - impaired muscle co-ordination (impairs manual skills)
  3. Tolerance and dependence
    - depends on frequency of use (tolerance develops faster for epilepsy than for use to induce sleep)
    - withdrawal effects, important to withdraw gradually
    - has abuse potential due to addiction
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16
Q

(not tested) Withdrawal effect of benzodiazepines

A
  • disturbed sleep
  • rebound anxiety
  • tremor
  • convulsions
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17
Q

(not tested) MOA of Zolpidem, a non-benzodiazepine

A

is a non-benzodiazepine

Also potentiates GABA A mediated Cl- currents at the same site as
benzodiazepines.

– Has good hypnotic effect, primarily used to treat INSOMNIA.
– Not effective as anxiolytics, not useful to treat anxiety disorder

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18
Q

(not tested) MOA of Buspirone, a non-benzodiazepine

A

is a non-benzodiazepine

  • exact MOA is unclear, but involves SEROTONIN AND DOPAMINE receptor system (not just GABA receptor system is involved in anxiety)
  • is a serotonin 5-HT1A receptor partial agonist, also binds dopamine receptors

– Indicated for GAD but anxiolytic effects takes 1-2 weeks.

– Lacks anticonvulsant and muscle relaxant properties. (as it does not work on GABA A receptors)

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19
Q

(not tested) MOA of Barbiturates, a IMPORTANT non-benzodiazepine

A

Also potentiate GABA A mediated Cl- currents, but at a site distinct from benzodiazepines (barbiturate site)

  • Not commonly used currently,
    due to its tendency to develop tolerance and dependence (even more than benzodiazepines)
  • HIGH ABUSE POTENTIAL
  • Severe withdrawal symptoms
  • Flumazenil not effective for treating barbiturate overdose (as barb does not bind to benzodiazepine site)
  • At very high does, they can directly open Cl channels as well as block Na+ channels. e.g. phenobarbital
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20
Q

(not tested) What are some long-acting barbiturates?

A

effect lasts for 1-2 days

usually used as anticonvulsants/antiepileptics
(but NEVER first-line, usually as a last resort)

e.g. phenobarbital

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21
Q

(not tested) What are some short acting barbiturates?

A

effect lasts for 3-8hrs

usually used as sedative and hypnotics

e.g. pentobarbital and amobarbital

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22
Q

(not tested) What are some ultrashort acting barbiturates?

A

effect lasts for 20 mins

Used for IV induction of anaesthesia

e.g. thiopental

23
Q

(not tested) MOA of Propanolol, a non-benzodiazepine

A

MOA: Beta-adrenergic receptor antagonist, is a beta-blocker

Used for treating performance anxiety and social phobias

Reduces physical symptoms associated with adrenergic activation (e.g muscle tremor, tachycardia)

Contraindicated in patients with asthma and heart conditions

24
Q

How do opioid analgesia work?

A

Plays on endogenous mechanism to:

  1. Inhibit propagation of pain signals
  2. Alter emotional perception of pain
  3. Elevate the pain threshold
25
Q

Sites of opioid receptors regulating pain includes:

A

Peripheral nociceptive terminals (peripheral analgesia)

The spine (spinal analgesia)

The brain (supraspinal analgesia)

26
Q

Three major opioid receptor types

A

µ (Mu)

δ (Delta)

κ (Kappa)

All 3 types belong to the G-protein coupled receptors

27
Q

Examples of functional effects of analgesia

A

Analgesia - Supraspinal
Analgesia - Spinal
Analgesia - Peripheral

Respiratory depression
Pupil constriction (Miosis)
Reduced GI motility
Euphoria
Dysphoria
Sedation
Physical dependence

28
Q

Which receptor mediates which effect?

A

Majority of functional effects are mediated by µ (Mu) receptors.

One exception: κ (Kappa) receptor mediates dysphoria (a state of unease or generalized dissatisfaction with life)

29
Q

Good to bad (fatal) effects of analgesia ranking

A

Peripheral Analgesia (good)
Spinal Analgesia
Cough suppression
Supraspinal Analgesia
Sedation
Reduced gut motility
Euphoria
Pupil constriction
Constipation
Dysphoria
Severe sedation
Respiratory depression (fatal)

30
Q

How does age affect the dosing of opioids?

A

Elderly patients usually require a lower dose to
achieve effective pain relief than younger patients.

31
Q

Which requires a higher opioid dose? Neuropathic or nociceptive pain?

A

Neuropathic pain usually requires higher opioid
doses than nociceptive pain.

Neuropathic pain: pain signals that arise from spinal-thalamic tract (nerves)

Nociceptive pain: arise from tissue damage

32
Q

What doses are required for continuous maintenance of pain relief?

A

Lower doses are usually required for continuous
maintenance of pain relief than administration in
response to recurrence of pain.

33
Q

Dosing to effect process for opioids

A
  • should be started at a low dose and carefully titrated until an adequate level of analgesia is obtained, or until persistent and unacceptable side effects
  • Failure of at least partial analgesia with incremental
    dosing in the opioid-naive patient may indicate that
    the pain syndrome is unresponsive to opioid therapy
  • For some patients with chronic pain, opioids do not
    exert an appreciable analgesic effect until a threshold
    dose has been achieved.
34
Q

What opioid agonists are used for analgesia purposes?

A

codeine, morphine, pethidine

35
Q

What opioid agonists are used for anaesthetic adjuvant (give together with another analgesic drug) purposes?

A

fentanyl

36
Q

What opioid agonists are used for cough suppressant/antitussive purposes?

A

codeine

37
Q

What opioid agonists are used for anti-diarrhoeal purposes?

A

diphenoxylate

note: this leads to opioid induced constipation

38
Q

What are some examples of strong opioid agonsists?

A
  1. Morphine
  2. Fentanyl
  3. Methadone
  4. Pethidine (merperidine)
39
Q

MOA and uses of Morphine

A

Strong µ (mu) agonist (weaker δ and κ agonist).

High maximum analgesic efficacy.

High liability for addiction/ abuse.

40
Q

MOA and uses of Methadone and Fentanyl

A

Strong µ agonists (no significant δ and κ affinity).

High maximum analgesic efficacy.

High liability for addiction/ abuse.

Note: Methadone is long-acting, Fentanyl is short-acting
(anaesthetic adjuvant).

41
Q

MOA and uses of Pethidine (meperidine)

A

Strong µ (mu) agonist (probably weaker δ and κ agonist).

SHORTER duration of action than morphine (useful as an epidural during labour as drug less likely to remain in neonate).

hallucinogenic and convulsant effects at high dose

Results in restlessness rather than sedation

Antimuscarinic effects (e.g. dry mouth, blurring of vision but no miosis and less spasm of smooth muscle)

42
Q

Examples of moderate opioid agonists

A

Codeine/dihydrocodeine
Tramadol

43
Q

MOA of codeine

A
  • Weak µ and δ agonist (probably not a κ agonist).
  • Low maximum analgesic efficacy.
  • Moderate liability for addiction/abuse.
  • When taken, is a low efficacy drug, but can be converted into a higher efficacy drug (morphine)
  • 10 % of population show reduced analgesic effect due to lack of demethylating enzyme (into morphine)
44
Q

MOA of tramadol

A
  • Weak µ (mu) agonist
  • Weak inhibitor of 5-HT and noradrenaline re-uptake

note: Ondansetron (anti-emetic) blocks analgesic effect

45
Q

Where does respiratory depression occur in the brain?

A

Nucelus tractus solitarius

Nucleus ambiguus

leads to:
- reduced responses to CO2 and H+
- suppressed voluntary breathing

Note: Opioids should be avoided in infants!

46
Q

What is the most important adverse effect of the use of opioids?

A

Respiratory depression

47
Q

Respiratory depression should not occur at
normal therapeutic
doses but can be lethal
in:

A
  • overdose
  • respiratory disease
  • hepatic dysfunction
  • combination with other CNS depressants
48
Q

Other common adverse effects arising from the use of opioids

A
  1. N&V
  2. Drowsiness (do not oeprate machinery/drive!)
  3. Constipation due to reduced GI motility (esp with chronic use)
  4. Miosis (pinpoint pupils) due to actions in the oculomotor
    nucleus. Is a diagnostic
    feature of opioid overdose.
  5. Urinary retention due
    to increased bladder
    sphincter tone
  6. Postural hypotension and
    bradycardia
  7. Immunosuppressant effect
    with long-term use
  8. Morphine can also trigger
    histamine release from
    mast cells:
    - urticaria and itching
    - bronchoconstriction
    - hypotension due to
    vasodilatation
    - to be used WITH CAUTION IN ASTHMATICS
49
Q

What is drug tolerance?

A

drug becomes less effective after prolonged use.

dose escalation required

50
Q

What is drug addiction?

A

psychological craving.

compulsive use.

loss of control over use.

51
Q

What is physical dependence?

A

physiological dependence
such that stopping the drug
leads to physical withdrawal
symptoms.

52
Q

Signs of opioid withdrawal

A
  • anxiety
  • irritability
  • chills
  • hot flushes
  • joint pain
  • lacrimation (tears), - rhinorrhea (runny nose),
  • nausea, vomiting
  • abdominal cramps
  • diarrohea
52
Q

How to treat opioid overdose?

A

Opioid antagonists —> Naloxone/Naltrexone/Nalmefene

Naloxone is short-acting (usually IV)

Naltrexone is long-acting (oral administration)

Nalmefene is long-acting (IV) new, most commonly used (replaced naloxone and naltrexone combo)

Note: Use with extreme caution in patients with
opiate dependency as they can precipitate potentially fatal withdrawal syndrome.

PPNP 3 (19 decks)

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