Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Narcotic analgesics and non-narcotic analgesics > Flashcards

Narcotic analgesics and non-narcotic analgesics Flashcards

1
Q

What type of drugs are narcotic analgesics?

A

Opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What group of drugs are non-narcotic analgesics?

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What proportion of visits to the doctor are due to pain?

A

60-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Should lecturers put weird philosophy stuff in their slides?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In order, what are the phases of pain?

A
  1. Transduction
  2. Transmission
  3. Perception
  4. Modulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the two general systems by which pain reception happens?

A

The nociceptive system and the antinociceptive system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the nociceptive system?

A

The system of pain reception and its physical appreciation with launching of some conditional and unconditional reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the antinociceptive system?

A

The system of excessive pain reception suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does the antinociceptive system exist?

A

Excessive pain perception can lead to distress and shock, so this system prevents such excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are first order pain afferents?

A

Neurones that, when triggered by a stimulus, conduct a pain signal to the spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are second order pain afferents?

A

Neurones that conduct a pain signal up the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are opiates and opioids?

A

OPIATE
Drugs derived from opium like morphine and codeine, and a wide variety of semi synthetic agents derived from them and from thebaine, another component of opium

OPIOID
A more inclusive term referring to all agonists and antagonists with morphine-like activity as well as to naturally occurring and synthetic opioid peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the term endorphin refer to?

A

Three families of endogenous opioid peptides: the enkephalins, dynorphins and beta-endorphins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What kind of receptors are opioid receptors?

A

G-protein coupled receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where in the synapse are opioid receptors located?

A

On the prejunctional neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the outcome of the effect of activated opioid receptors?

A

Inhibition of release of neurotransmitters noradrenaline, dopamine, GABA, 5-HT ad glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the molecular process between activation of opioid receptors and their final effect

A

Activation reduces intracellular cAMP formation
Opening of K+ channel via μ and δ
Suppression of N-type Ca++ channels

Ultimately hyperpolarisation and reduced intracellular Ca++
Reduced neurotransmitter release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three types of opioid receptor?

A

Delta, kappa and mu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are delta, kappa and mu opioid receptors found in the body?

A

Delta - Brain
Kappa - Brain, spinal cord
Mu - Brain spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the therapeutic effects of activation of the three types of opioid receptor?

A

DELTA - Analgesia, antidepressant effects, physical dependence

KAPPA - Spinal analgesia, sedation, miosis, inhibition of anti-diuretic hormone release

MU1 - Supraspinal analgesia, physical dependence

MU2 - Respiratory deression, miosis, euphoria, reduced GI motility, physical dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are narcotic agents traditionally classified?

A

STRONG - morphine, diamorphine, fentanyl

INTERMEDIATE - partial agonists, mixed agonist-antagonist

WEAK - codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are narcotic agents structurally classified?

A

MORPHINANS - morphine, codeine

PHENYLPERIDINES - meriperidine, fentanyl

DIPHENYLPROPHYLAMINES - methadone, dextropropoxyphene

ESTERS - remfentanil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are narcotic agents functionnally classified?

A

PURE AGONISTS - morphine, codeine

PARTIAL AGONISTS - buprenorphrine

MIXED ACTION - pentazocine, nalbupine, butorphanol

ANTAGONISTS - naxolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What side effects of narcotic analgesics does the mnemonic MORPHINE stand for?

A 
M - miosis
O - orthostatic hypotension
R - respiratory depression
P - physical dependency
H - histamine release
I - increased ICP
N - nausea
E - euphoria
S - sedation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the analgesic action of morphine

A

Two components: spinal and supraspinal

Inhibits release of excitatory transmitters from primary afferents - at substantia gelatinosa of dorsal horn

Exerted through interneurones - gating of pain

At supraspinal level in midbrain, cortex and medulla - alter processing and interpretation and send inhibitory impulses through descending pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the sedation caused by morphine

A

Drowsiness and indifference to surroundings

Inability to concentrate and extravagant imagination - colourful daydream

Apparent excitement

Larger doses produce sleep - EEG resembles normal sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the mood effects of morphine

A

In normal persons calming effect, mental clouding, feeling of detachment, lack of initiative etc - unpleasant in absence of pain

Sometimes dysphoria

But in persons with pain and addicts sense of wellbeing, pleasurable floating sensations - kick euphoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the depressive actions of morphine

A

Respiratory centre depression - both rate and depth of depression are diminished - dangerous in head injury and asthmatics

Cough centre depressed

Temperature centre regulation depressed

Vasomotor centre - high doses cause fall in blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the stimulating effects of morphine

A

CTZ (cranioreceptor trigger zone) - sensitize CTZ to vestibular and other impulses

Edingher Westphal Nucleus - miosis

Vagal centre - bradycardia

Hippocampal cells - convulsions (inhibition of GABA release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the effect of morphine on the gastrointestinal tract

A

Constipation due to direct action on the intestine reducing propulsive movement, spasm of sphincters, decrease in all GIT secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the effect of morphine on the smooth muscles

A

Biliary tract - biliary colic, closure of sphincter of Oddi

Bladder - urinary urgency but difficulty

Bronchi - bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the therapeutic uses of morphine?

A
  1. Long bone fracture
  2. Myocardial infarction
  3. Terminal stages of cancer
  4. Burn patients
  5. Visceral pains - pulmonary embolism, pleurisy, acute
    pericarditis
  6. Biliary colic and renal colic
  7. obstetric analgesia
  8. Segmental analgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the side effects of morphine?

A
  1. Respiratory depression (infant and old)
  2. Vomiting
  3. Sedation, mental clouding - sometimes dysphoria
  4. Hypotensive effect
  5. Rise in intracranial pressure
  6. Apnoea: new born
  7. Urinary retention
  8. Idiosyncrasy and allergy
  9. Acute morphine poisoning
  10. Tolerance and dependence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What dose of morphine causes acute poisoning?

A

> 50mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What dose of morphine is lethal?

A

> 250mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is morphine overdose managed?

A

Gastric lavage with potassium permanganate (KMNO4)

Antidote is Naloxone 0.4-0.8mg every 2-3 minutes until respiration picks up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the danger of repeated morphine use?

A

Psychological dependence

Physiological dependence

Tolerance

Withdrawal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How long do short- and long- acting opiates have an effect?

A

Short - 6 to 12hrs

Long - 30hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the symptoms of opiate withdrawal?

A 
Nausea
Vomiting
Stomach cramps
Diarrhoea
Goosebumps
Depression
Drug cravings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Where does Tramadol act?

A

Centrally acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How strongly does Tramadol stimulate opioid receptors?

A

Very weakly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does Tramadol reduce pain?

A

Other mechanisms involved in analgesic action

NA reuptake inhibition - spinal inhibition of pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What routes of administration are effective for Tramadol?

A

Oral and IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do the side effects of tramadol compare to those of morphine?

A

Similar but less severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How well tolerated is tramadol?

A

Well tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How much abuse potential is there for tramadol?

A

Low abuse potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How well does naloxone reverse the action of tramadol?

A

Only partially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is tramadol used for?

A

Neuropathic pain and short diagnostic procedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the normal dose of tramadol?

A

50-100mg IV/IM/oral

50
Q

What receptors do pure opioid antagonists have affinity for?

A

All opioid receptors - delta, kappa and mu

51
Q

What can opioid antagonists do to opioids bound to alpha-receptors?

A

Displace them

52
Q

What is the effect of opioid antagonists on normal people, poisoned people and addicts?

A

Normal - no effect

Poisoned people - reverses poisoning

Addict - relieves withdrawal symptoms

53
Q

What is the mechanism of action of pentazocine?

A

Weak alpha-receptor antagonist but agonist of kappa-receptor

54
Q

How frequently is pentazocine used?

A

One of the commonly used agents

55
Q

How is pentazocine administered?

A

Orally and IM

56
Q

How liable is pentazocine to be abused?

A

Low abuse liability

57
Q

Describe the pharmacokinetics of pentazocine

A

High first pass metabolism but effective orally

Metabolised in the liver by glucoronide conjugation

Half life = 3-4hrs

58
Q

What is the normal dose of pentazocine?

A

Orally 50-100mg

IM 30-60mg

59
Q

What is pentazocine used for?

A

Moderately severe pain in:

Injury
Burns
Fracture trauma
Cancer
Orthopaedic manoeuvres
60
Q

What are the features of pentazocine compared to morphine?

A

Spinal analgesia via kappa receptor

Dose is 30mg vs 10mg and low ceiling effect

Sedation and respiratory depression at lower doses

Tachycardia and rise in BP - dangerous in MI

Lesser smooth muscle spasms

Vomiting and other side effects are less

Subjective effects - lower ceiling (psychomimetic
effects)

Tolerance develops on repeated use but less than morphine

Withdrawal symptoms - similar to morphine

Good analgesic in subjects not exposed to morphine

Precipitate withdrawal - in morphine addicts

61
Q

What is the origin of Buprenorphine?

A

Synthetic thebaine cogener

62
Q

Is Buprenorphine lipid or water soluble?

A

Highly lipid soluble

63
Q

How is Buprenorphine administered and why?

A

Sublingually and parenterally but not orally because of its high first pass metabolism

64
Q

What is the mechanism of action of Buprenorphine?

A

Selective mu receptor agonist

65
Q

How does the potency of buprenorphine compare to morphine

A

20-30 times greater than morphine

66
Q

How does the duration of action of buprenorphine compare to that of morphine?

A

Slower to take effect but lasts longer - up to 24hrs

67
Q

Describe the pharmacological effects of buprenorphine

A

Similar to morphine

68
Q

What is the ceiling effect?

A

The drug ceiling effect refers to a particular phenomenon in pharmacology where a drug’s impact on the body plateaus. At this point, taking higher doses does not increase its effect. It has, in essence, hit a ceiling. This happens with many types of drugs, including aspirin and opioids.

69
Q

Does buprenorphine have a ceiling effect?

70
Q

What kind of patients is buprenorphine suitable for?

A

Patients who are new to opioids or don’t take them regularly

Unsuitable for addicts - precipitates withdrawal symptoms

71
Q

How does tolerance of buprenorphine compare to that of morphine?

72
Q

How does the chance of physical dependence of buprenorphine compare to that of morphine?

73
Q

How does the liability for abuse of buprenorphine compare to that of morphine?

74
Q

Describe the withdrawal symptoms of buprenorphine

A

Similar to morphine

75
Q

Give the adverse effects of buprenorphine

A

Postural hypotension

Respiratory depression (fatal in neonates and cannot be reversed by naloxone)

76
Q

Give the uses of buprenorphine

A

Long-lasting painful conditions - cancer

Post-operative pain

Myocardial infarction

77
Q

What preparations are available for buprenorphine?

A

Norphine, Tidigesic

0.3 mg/ml injections and 0.2 mg sublingual tablets

78
Q

How does overdose of narcotics happen?

A

Tolerance develops and dose is gradually increased to compensate until there is an overdose

79
Q

What are the symptoms of opioid poisoning?

A

CNS - coma, convulsions

CARDIAC - hypotension, bradycardia

RENAL - urinary retension

PULMONARY - bradypnoea, Cheyne-Stokes respiration
(hyperpnoea, hypopnoea, apnoea,
repeat)

EYES - miosis

80
Q

Give the supportive measures in opioid poisoning

A

Maintain patent airway

Endotracheal intubation - ventilation

Activated charcoal

81
Q

Give the antidotes to opioid poisoning

A

Naloxone - all opiates except buprenorphine

Naltrexone

Nalmefene

82
Q

Give the mechanism of action of naloxone

A

Competitive antagonist of all opioid receptors

Inhibits mu receptors at a much smaller dose

83
Q

How is naloxone administered?

84
Q

Which symptoms of morphine action does naloxone inhibit?

A

All of them

85
Q

Compared to morphine what needs to be done with the dose of naloxone to antagonise the action of nalorphine and pentazocine?

A

Higher doses

86
Q

Does naloxone antagonise all the actions of nalorphine and pentazocine?

A

No

Dysmorphic and psychomimetic effects are not suppressed (delta receptors)

87
Q

What doses of naloxone need to be given to alleviate withdrawal symptoms of marphine, nalorphine and pentazocine?

A

0.4mg doses - morphine

4-5mg doses - nalorphine and pentazocine

88
Q

What is the basic mechanism of action of all NSAIDs?

A

Inhibiting cyclooxygenase (COX1, COX2) and thus inhibiting formation of prostaglandins

89
Q

Is the action of NSAIDs reversible?

A

Only for aspirin

90
Q

What are the functions of prostaglandins?

A 
Induce sleep
Reduce intraocular pressure
Vasodilation
Bronchodilation
Prevent arterial sclerosis
Production of gastric mucus
Maintain renal circulation
Promoting uterine contraction 
Prevents arthritis
91
Q

What are the mechanisms of action of COX1 and COX2?

A

COX1 is responsible for the production of physiological production of prostanoids

COX2 is responsible for the production of prostanoids in sites of disease and inflammation

92
Q

What is the function of COX1

A

It is described as the housekeeping enzyme that regulates normal cellular processes such as gastric cytoprotection, vascular cytoprotection, platelet aggregation and kidney function

93
Q

What is the function of COX2?

A

Expression is increased during states of inflammation

94
Q

What s the function of COX3?

A

Increasing of pain impulse transmission through afferent pathways

Influence upon centre of thermoregulation (decreasing of warm eradiation)

95
Q

In terms of effects, what are the two types of non-selective COX1 and COX2 inhibitors?

A

Those with equal analgesic, anti-inflammatory and anti-pyretic properties

Those with Mainly anti-inflammatory effect

96
Q

What are the therapeutic effects of NSAIDs and how do they come about?

A

Anti-inflammatory
Analgesic
Antipyretic
Spasmolytic

Due to COX2 inhibition

97
Q

What are the effects of NSAIDs that are therapeutic or adverse depending on the situation?

A

Anti-platelet
Tocolytic
Spasmolytic

98
Q

What are the adverse effects of NSAIDs and how do they come about?

A 
Ulcerative
Chondrotropic, osteotropic
Haematotoxic
Hepatotoxic
Nephrotoxic
Cardiotoxic
Cerebrotoxic

Mainly COX1 inhibition

99
Q

How are NSAIDs thought to produce their analgesic effect?

A

Prostaglandins are thought to sensitise nerve endings to inflammatory mediators. Therefore by reducing prostaglandin formation through COX inhibition, NSAIDs reduce pain

100
Q

What kind of pain are the salicylate NSAIDs used for?

A

Low to moderate severity arising from musculoskeletal disorders

101
Q

Name conditions in which NSAIDs are used

A

Rheumatoid arthritis and osteoarthritis

102
Q

How is fever related to the NSAIDs?

A

Fever is produced when an inflammatory process produces endogenous pyrogenic agents which stimulate the production of prostaglandins which increase the set point of the hypothalamus, thus causing fever.

By inhibiting prostaglandin production, NSAIDs reduce fever

103
Q

How do NSAIDs reduce inflammation?

A

Inhibition of prostaglandin production reduces aspects of inflammation in which prostaglandins are mediators

104
Q

Can aspirin arrest the progress of arthritis or induce remission?

105
Q

How can NSAIDs be used for the treatment of patent ductus arteriosus?

A

It is the cessation of production of prostaglandins that normally closes the ductus arteriosus

Small doses of aspirin or indomethacin mimic this effect and cause closure in most cases

106
Q

Give clinical uses of NSAIDs

A

For prevention of attack of MI (prevent platelet aggregation)

For relief of dysmenorrhea

For gout in high dose

107
Q

Give the adverse GI effects of NSAIDs

A 
Epigastric distress
Nausea
Vomiting 
Erosions
Ulceration
GI bleeding
108
Q

How do NSAIDs cause GI issues?

A

Reduced prostaglandins increase acid production, reduce bicarbonate production, reduce mucus production and reduce trophic effects on mucosal cells.

109
Q

How can GI symptoms of NSAIDs be reduced?

A

Use COX2 specific NSAIDs

Limit duration of therapy as much as possible

Limit dose as much as possible

110
Q

Give the renal disorders caused by NSAIDs

A 
Salt and fluid retention
Hypertension
Interstitial nephritis
Nephrotic syndrome 
Acute renal failure
Acute tubular necrosis
111
Q

How do NSAIDs cause renal adverse effects?

A

Changes in renal haemodynamics cause by a reduction in prostaglandins which normally cause a widening of the afferent arterioles

112
Q

What are the adverse effects of NSAIDs on blood?

A

Prolonged bleeding time due to reduced platelet aggregation

113
Q

How should NSAIDs be managed if a patient requires surgery?

A

Aspirin should be stopped 1 week before surgery

114
Q

What is the metabolic side effect of NSAIDs?

A

Hyperthermia?

115
Q

How do NSAIDs cause hyperthermia?

A

In toxic quantities they cause energy that normally goes towards producing ATP to be dissipated as heat

116
Q

What percentage of people given NSAIDs experience a hypersensitivity reaction?

A

15% (including me!)

117
Q

What is Reye’s syndrome?

A

Fulminating liver failure with cerebral oedema when aspirin or other salicylates are given during a viral infection, most commonly seen in children

118
Q

In children what should be used to reduce fever in order to avoid risk of Reye’s disease?

A

Acetaminophen
or
Ibuprofen

119
Q

What are the symptoms of mild salicylism (salicylate poisoning)?

A 
Nausea
Vomiting
Marked hyperventilation
Headache
Mental confusion
Dizziness
Tinnitus
120
Q

How dangerous can salicylates be in children?

A

Ingestion of as little as 10mg can be lethal

Pharmacology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions