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Primary Pharmacology > Antiemetics and aperients > Flashcards

Antiemetics and aperients Flashcards

1
Q

Where is the chemoreceptor trigger zone

A

Area postrema on the floor of the 4th ventricle bilaterally

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2
Q

What receptors in particular are prominent at the chemoreceptor trigger zone

A

Dopamine 2 receptors
5HT3
ACh

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3
Q

Phenothiazines examples

A

Propylamine
Piperidine
Piperazine
Chlorpromazine
Thioridazine
Prochlorperazine

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4
Q

What class do phenothiazines come from?

A

Dopamine antagonists

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5
Q

Chlorpromazine is sometimes also known as?

A

Largactil

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6
Q

Chlorpromazine MOA

A

Dopamine antagonist - D2
Muscurinic recepotr antagonist
Noradrenergic alpha 1 and 2 antagonist
Histamine 1 antagonist
Seratonin antagonist
Membrane stabilising properties
Prevents noradrenaline uptake into sympathetic nerves
CNS - isolating the reticular activating system from afferent connections resulting in sedation, disregard of external stimuli and reduction in motor activity

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7
Q

Chorpromazine effects including side effects

A

CNS - EPS due to central dopamine antagonism, NMS occurs rarely, variable effects on hypothalamic function, reducing secretion of grwoth hormone while increased release of prolactin, temperature regulation altered and can result in hypothermia

CV - peripheral vasodialtion, hypotension, increased heat loss
Anticholinergic
Gut - increased appetite, weight gain
Misc - contact sensitivsation, cholestatic jaundice, agranulocytosis, leucopenia, leucocytosis, haemolytic anaemia

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8
Q

Chlorpromazine kinetics

A

Absorption - good, large hepatic first pass metabolism limits its bioavailability to 30%. IV available
Distribibution -
Large number of hepatic metabolites in the urine or bile
Variable but small fraction unchanged in the urine

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9
Q

Prochlorperazine vs chlorpromazine vs droperidol vs metoclopramide vs domperidone in sedation, anticholinergic effects and EPS

A
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10
Q

Prochlorperazine effects

A

CNS - extrapyramidal effects are seen more commonly than other dopamine antagonists, dystonias and akasthesia partcularly, children and young adults more commonly effected. When used perioperatively produces mild sedation
Cholestatic jaunice, haematological abnormalities, skin sensitisation, hyperprolactinaemia and rarely NMS

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11
Q

Prochloperazine kinetics

A

Absorption - erratic, oral bioavailability very low due to extensive first pass metabolism
IV and IM available

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12
Q

Droperidol belonds to which class of dopamine antagonsits?

A

Butyrophenone

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13
Q

Droperidol MOA

A

Antagonists D2 receptors at the CTZ

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14
Q

Droperidol side effects

A

CNS - sedation more pronounced, EPS side effects more with larger doses, may develop >12 hours post administration and up to 25% experience anxiety up to 48 hours after administration
Hyperprolactinaemia
CV - hypotension from peripheral alpha adrenoreceptor blockade
QT prolongation

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15
Q

Droperidol kinetics

A

IV alhough absorbed readily from IM
Highly plasma protein bound 90%
Extensively metabolised by the liver to products excreted in urine
Only 1% of drug excretion is as unchanged drug in urine

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16
Q

Domperidone different to other dropamine antagonists, how does this effect side effects

A

does not cross BBB
Reduced EPS

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17
Q

Metoclopramide belongs to which class of dopamine antagonsits?

A

Benzamides

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18
Q

Benzamide example

A

Metoclopramide

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19
Q

How effective is metoclopramide as an antiemetic?

A

as placebo in 50% of studies

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20
Q

MOA of metoclopramide

A

dopamine 2 receptor antagonism at the CTZ and prokinetic effects at the tstomach, also blocks 5HT3 receptor

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21
Q

Metoclopramide effects

A

CNS - crosses BBB, EPS side effects seen up to 72 hours post administration, more common in young females 1:5000, NMS possible. Agitation sometimes seen
CV - hypotension,. tachycardia or bradycardia if rapid administration

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22
Q

Metoclopramide pharmacokinetics

A

Well absorbed
First pass metabolism varies significantly with 30-90% bioavailability
IV or IM
Conjugated in liver and excreted unalong with unchanged drug in urine

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23
Q

What is an example of a tertiary amine anticholinergic?

A

Atropic
Hyoscine

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24
Q

Chemically atropine is?

A

Tertiary amine - esters formed by combination of tropic acid and organic base (tropine) and are abel to cross BBB

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25
Q

How is glycopyrrolate different in structure and therefore action to atropine?

A

Synthetic quaternary amine as opposed to tertiary amine - this means it is charged and unable to cross the BBB with no central effects

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26
Q

Hyoscine comes in what combination?

A

Raecaemic - only hyoscine I is active

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27
Q

Hyoscines effects

A

Central - anticholinergic syndrome (excitement, ataxia, hallucinations, behavioural abnormalities

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28
Q

Compare hyoscine, atropine and glycopyrlolate in terms of their
- Antiemetic potency
- Sedation/amnesia
- Anti-sialogogue
- Mydriasis
- Placental transfer
- Bornchodilation
- heart rate

A
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29
Q

Hyoscine pharmacokinetics

A

variable absorptiopn, oral bioavailability between 10-50%
Transdermal administration effective despite low plasma levels
Extensively metabolised by liver esterases and only small fraction excreted unchanged in urine
Duration of action shorter than atropine

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30
Q

Atropine preparation includes

A

Raecemic mixture
Only 1 - atropine is active

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31
Q

Atropine effects

A

CNS - sedative, can cause central cholinergic crisis
CV - initial bradycardia due to central effects on vagal nucleus, or reflecting partial agonist effect at cardiac muscurinic receptors
Respiratory - bronchodilation, increased dead space, reduced secretions
GIT - less effective antisialogogue than hysocine, tone of lower oesophageal sphincter decreased, small decrease in GIT secretion
Misc - sweating inhibited, may provoke pyrexia in paediatric patients, increase intra ocular pressure

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32
Q

Atropine pharmacokinetics

A

Intestinal absorption rapid, unpredictable levels
50% plasma protein bound
Extensively metabolised by liver esterases
Excreted in urine (tiny fraction unchanged)

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33
Q

Glycopyrolate pharmacokinetics

A

Intestinal absorption negligibale
Oral bioavailability <5%
Does not cross BBB
Minimally metabolised and 80% excreted unchanged in urnie

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34
Q

Cyclizine MOA

A

histamine 1 antagonist with anticholinergic properties that may contribute to its antiemetic actions

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35
Q

Cyclizine chemically

A

piperazine derivative

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36
Q

Cyclizine IV beware

A

Prepared with lactic acid at pH 3.2 and can be painful, particulaly intramuscular dosing

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37
Q

Cycliznie effects

A

Gut - increases lower oesophegeal sphincter tone
Anticholinergic - mild
EPS rarely

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38
Q

Cyclizine kinetis

A

Well absorbed orally and high oral bioavailability 75%
Little is known regarding the rest fo the kinetics

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39
Q

Ondansetron belongs to what class and subclass

A

5HT3 antagonists
Carbazole

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40
Q

Ondansetron available in what preparations?

A

Tablets, SL, suppository, clear solution for slow IV injection

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41
Q

MOA of ondansetron

A

Peripehral 5HT3 and central 5HT3 antagonism

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42
Q

Side effects of ondansetron

A

headache, flushing, constipation, bradycardia

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43
Q

Pharmacokinetics of ondansetron

A

Well absorbed with oral bioavailability 60%
75% protein bound
Signficiant heptatic metbaolism by hydroxylation and subsequent glucoronide conjugationto inactive metabolites
Half life 3 hours
Dose should be reduced in hepatic imapirment

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44
Q

Aprepitant belongs to which class

A

NK1 receptor antagonists

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45
Q

Name a neurokinin 1 receptor antagonist

A

Aprepitant, fosaprepitant

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46
Q

NK1 receptor antagonist MOA

A

Block the actions of substance P in the brain stem nuclei of the dorsal vagal complex central to the regulation of vomiting

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47
Q

Aprepitant is adminsitered how?

A

oral

48
Q

Fosaprepitant is adminsitered how?

A

IV prodrug

49
Q

Pharmacokinetics of aprepitant

A

Bioavbailability 60%
97% plasma protein bound
Metabolised by CYP3A4 to weakly active metbaolites excreted in urine and faeces

50
Q

Dexamethasone antiemetic actions potentiated most when?

A

Prevention of post operative vomiting
Not effective in established vomiting

51
Q

How much dexamethasone is effective for vomiting?

A

4mg as effective as higher doses

52
Q

MOA of dexamethasone as an antiemetic

A

Not well understood
May involve prostalganding antagnoism
Releas eof endorphins - appetitie stimulation and release of endorphis
Antiinflammatory effect reducing gut seratonin release

53
Q

Nabilone is what type of antiemetic

A

cannabinoid

54
Q

Which benzodiazepine has some action as an antiemetic

A

Lorazepam
Mode of action uncertain

55
Q

Metoclopramide is from what class of dopamine antagonsits?

A

Benzamide

56
Q

Antemetic activity of metoclopramide

A

D2 receptor antagonist - CTZ - primary action
5HT3 antagonist at high doses
Decrease in sensitivity of visceral aferrants for supply of information to the vomiting centre

57
Q

Metoclopramide has additional actions beyond its antiemetic activity through? Describe its MOA for this effect

A

Prokenitic

Selective stimulation fo gastric muscurinic receptors causing prokinetic activity
peripheral D2 receptor antagonist causing prokinetic activity
5HT4 AGONIST causing prokinetic activity
Direct action on smooth muscle to icnrease tone

58
Q

What effect on gastric motility does metoclopramide have”

A

inreased gastric emptying - a,plitude of gastric contractions increases, accelerates small intestinal transit time, variable effects on large bowel motility
Increased lower oesophageal spincter tone
No effec ton gastric secretions

59
Q

Major side effects of metoclorpamide

A

EPS - up to 72 hours after adminsitration
Akasthesia - inner restlessness
Sedation
Oculogyric crises
NMS
Hyperprolactinaemia
CVS - tachycardia or bradycardia, hypetnesion or hypotension

60
Q

Contraindications to metoclopramide

A

Porphyria

61
Q

Oral bioavailability of metoclopramide

A

30-90%
Variable first pass metabolism - first pass metabolism with sulfate conjugation
Rapidly absorbed

62
Q

Ondansetron comes from what class

A

Synthetic carbazole

63
Q

Ondansetron acts where?

A

selective antagonsit of 5HT3 at CTZ and gut

64
Q

What interactions does ondansetron have

A

reverses soe analgesic effects of tramadol

65
Q

Side effects of ondansetron?

A

Headache
FLushing
Constipation - large bowel transit time

Uncommon
- LFTs increase
- Hypotension, bradycardia
- Hypersensitivity
- prolonged QT

66
Q

Ondansetron pharmacokinetics

A

Absorption - passively and completely
Oral bioavailability - 60%
Peak plasma concentrations 1.5 hours orally
Protein binding - 75%
Vd 2L/kg
Significant hepatic metabolism by CYP 450 (3A4, 2D6, 1A2) by hydroxylation or demethylation followed by conjugation with glucoronide or sulfate . No dose adjustment for interactions due to multiple enzymatic routes of emtabolism
Inactive metabolites
Renal excretion - <5% unchanged
Half life 3 hours

67
Q

Granisetron MOA

A

Selective antagonsit at 5HT3 CTZ and gut

68
Q

Granisetron SE

A

Headache
FLushing
Constipation

Uncommon
- LFTs increase
- Hypotension, bradycardia
- Hypersensitivity
- prolonged QT

69
Q

Pharmacokinetics of granisetron

A

demethylation by CYP450
Excreted in urine and facecs
Half life 9 hours

70
Q

Ondansetron presentation

A

Clear colourless aqueous solution in ampoules of 4ml, tablets and SL

71
Q

ONdansetron vs critical illness

A

Renal failure - no change required, despite delayed clearance has inactive metbaolites
Hepatic failure - near 100% oral bioavailability, signfiicantly reduced clearance and dose reduction to 8mg per day advised

72
Q

Chemical structure of metoclopramide

A

Chlorinated procainamide derivatve

73
Q

Presentations of metaclopramide

A

10mg tablets, syrup, clear colourless solution

74
Q

Metaclopramide pharmacokinetics

A

Absorption - rapid, near complete. Oral bioavailability however is 30-90% due ot sulfate conjugation
Distribution 20% pritein bound, Vd 2.5L/kg
Metbaolism - liver - sulfate derivative metbaolite
Excretion - 80% of oral dose excreted in urine within 24 hours., 20% unchanged, remainder appears as non metabolised drug conjugated to sulfate or glucoronide
Elimination half life 3-5 hours
Not removed by haemodialysis

75
Q

Droperidol is chemically derived from?

A

Butyrophenone

76
Q

Droperidol main actions and MOA

A

Antiemetic and neuroleptic

Central dopamine D2 blockade at CTZ
Post synaptic GABA antagonism

77
Q

Methods of droperidol adminsitration

A

Oral
IM
IV

78
Q

Droperidol effects
- CVS
- Respiratory
- CNS
- Abdominal
- Metabolic

A

CVS - minimal, some antagonistic effects at alpha adrenergic receptors leading to hypotension if hypovolaemia coexistent
Resp - decreased minute volume and FRC and airway resistance decreases
CNS - neurolepsis, diminished motor activity, anxiolysis, indifference. Seizure threshold raised
Abdominal - antiemetic
Metabolic -= hyperprolactinaemia
Reduces total body oxygen consumption

79
Q

Droperidol SE

A

EPS - 1%
LFT abnormalities
Allergic rare
NMS

80
Q

Droperidol kinetics

A

Absorption - well absorbed IM, oral absorption not elucidated
Distribution 90% protein bound, Vd 2L/kg
Metabolism - extensively metabolised in the liver, oxidative dealkylation
Excretion - 75% excreted in urine, 1% unchanged, 22% in faeces
Clearance 10-18 ml/min/kg
Elimination half life 2 hours

81
Q

Prochlorperazine is otherwise known as?

A

Stemetil

82
Q

Prochlorperazine chemically derived from

A

phenothiazine of the piperazine subclass

83
Q

Preparations of prochloperazine

A

tablets
Sippositories
Clear colourless IV injection

84
Q

Prochlorperazine MOA

A

Dopamine antagonsim centrally

85
Q

Effects of prochlorperazine
- CVS
- Respiratory
- CNS
- Abdominal
- Metabolic

A

CVS - orthostatic hypotension secondary to alpha adrenergic blockade, ECG changes including prolonged QTc
Respiratory - mild respiratory depression
CNS 0 neuroleoptic
Abdominal - lower oesophageal tone increased
Metabolic - antiadrenergic, antiinflammatory, antipruritic, anticholinergic, anti histaminergic

86
Q

Prochlorperazine side effects

A

EPS
Jaundice
Leucopenia
Rashes
NMS

87
Q

NMS side effects would appear as?

A

Catatonia
CV lability
Hyperthermia
Myoglobulinaemia

88
Q

Prochloperazine pharmacokinetics

A

Absorption - slow, 0-16% bioavailability
Distribution - highly protein bound 90%, Vd 20L/kg
Metabolism - first pass metabolism ++, CYP3A4 and CYP2D6 S oxidation to a sulfoxide
Half life 6-8hours

89
Q

Promethazine chemically

A

Phenothiazine

90
Q

Promethazine main actions

A

Antihistaminergic
Sedative
Antiemetic

Reversible competitive antagonsit at H1 histaminergic receptors
Anticholinergic
Anti serotonergic
Anti dopaminaergic

91
Q

Effects of promethazone
CVS
Resp
CNS
Abdominal

A

CVS - rapid intravenous adminsitration causing hypotension
Resp - bronchodilation, reduces respiratory tract secretions, antitussive
CNS - sedative, anxiolytic, slight antanalgesic, reduces motion sickness by vestibular end organ recepotr and inhibitor actions at CTZ.
Abdominal - decreases tone of lower oesophageal sphincter

92
Q

Promethazine side effects?

A

Anticholinergic
EPS
Jaundice
Photosensitivity
Excitatory phenomena

93
Q

Promethazine kinetics

A

Absorption - well absorbed, extensive first pass metabolism
Distribution 90% protein bound, Vd 2.5L/kg
Metabolism - sulfoxidation and N dealklylation in the liver
Excretion - urine, 2% unchanged
Clearance 1L/min
Eliomination half life 10 hours

94
Q

Dopamine antagonists which act as antiemetics include what classes

A
  • Phenothiazines (Chlorpromazine/prochlorperazine - Stemetil), which also have potent activity against muscarinic, H1, 5-HT3 and dopamine receptors
  • Butyrophenones (droperidol), which have slightly less potent anticholinergic, 5HT3 blockade and antihistamine effects - haloperidol faster antiemetic than droperidol IM, similar IV
  • Benzamides (metoclopramide), which have a prokinetic effect related to indirect cholinergic activity, cleanest dopamine blockade D2
    ◦ Mild action at H1 receptors, strong D2 blockade, mod 5HT3 blockade
95
Q

What characteritises phenothiazines as antiemetics

A
  • Phenothiazines (Chlorpromazine/prochlorperazine - Stemetil), which also have potent activity against muscarinic, H1, 5-HT3 and dopamine receptors
96
Q

What MOA characteristics do you find of butyrophenones as antiemetics? e.g.

A
  • Butyrophenones (droperidol), which have slightly less potent anticholinergic, 5HT3 blockade and antihistamine effects - haloperidol faster antiemetic than droperidol IM, similar IV
97
Q

Metoclorpramide belongs to which class of dopamine antiemetics? What characterises this class? What actions does it have

A
  • Benzamides (metoclopramide), which have a prokinetic effect related to indirect cholinergic activity, cleanest dopamine blockade D2
    ◦ Mild action at H1 receptors, strong D2 blockade, mod 5HT3 blockade
98
Q

Anticholinergic antiemetics include? 3 side effects

A
  • Hyoscine, atropine (purely antimuscarinic)
  • Phenothiazines and butyrophenones also have strong antimuscarinic effect
  • Side effects
    ◦ Hallucinations
    ◦ Drying of secretions - dry mouth, dry eyes, constipation
    ◦ Central - anticholinergic syndrome (excitement, ataxia, hallucinations, behavioural abnormalities
99
Q

5HT3 antagonists as a class include? What other agents are potent at this receptor

General side effects of this class

A

5-HT3 antagonists:
* ondansetron and granisetron are pure, high-affinity 5-HT3 antagonists
* Phenothiazines and butyrophenones also have strong 5-HT3 antagonist effects
* SE - constipation, headache, LFT

100
Q

Antihistamine antiemetics include?
Side effects
MOA

A
  • Promethazine, Cyclizine and prochlorperazine have mainly anti-H1 effects
    ◦ promethazine - Phenergen - dominant histamine and dopamine blockade with some muscurinic action also. Could be in the phenothiazine group
  • Most centrally acting H1 antagonists also have potent antimuscarinic activity
  • Side effects
  • drowsiness
101
Q

What is aprepitant

A

NK1 antagonist

102
Q

Miscellaneous antiemetics include

A

Propofol
Dexametjasone
Cannabindois
Benzos

103
Q

Metoclopramide pharmacodynamics 4

A

◦ Selective stimulation of gastric muscurinic receptors causing prokinetic activity
◦ peripheral D2 receptor antagonist causing prokinetic activity
◦ 5HT4 AGONIST causing prokinetic activity
◦ Direct action on smooth muscle to increase tone

104
Q

oeosphageal effects of metoclopramide

A

◦ Increased amplitude of oesophageal perstaltic contractions (though not every study is able to demonstrate this effect)
◦ Increased resting tone of the lower gastro-oesophageal sphincter (a short-term effect, lasting approximately one hour)

105
Q

gastric effects of metoclorpamide

A
  • Gastric effects:
    ◦ Accelerates gastric emptying, including the scenarios of diabetic and post-operative gastroparesis - this is described by the college as “appears to depend on intramural cholinergic neuron”. In actual fact it appears to be an indirect effect, where metoclopramide enhances the acetylcholine release from suitable nerve endings (Sanger, 1985)
    ◦ Increased antral contractions
    ◦ Improved “antroduodenal coordination” (Lee & Kuo, 2010)
    ◦ No effect on gastric secretion
  • Intestinal effects
    ◦ Increases the peristaltic activity of the upper small intestine - speeding intestinal transit time
106
Q

Antiemetic general rules
- Formulations
- Bioavailability
- Vd
- Protein binding
- Metabolised
- Half lives
- Qt

A
  • Oral formulations are available for all of them, even though it makes no sense to force a vomiting nauseous person to ingest a tablet.
  • Most of them have good oral bioavailability, the exceptions being prochlorperazine and domperidone
  • They all have modest volumes of distribution, except domperidone which behaves a bit like amiodarone
  • They are all highly protein-bound, except for metoclopramide and hyoscine.
  • They are all metabolised by the liver. Of these, the only exception is metoclopramide, of which 20-50% is renally eliminated.
  • Their half-lives do not usually reflect the duration of their effect (for example, the effects of aprepitant last for 48 hours, but its half-life is 9-13 hours).
  • The vast majority of them prolong the QT interval. It would actually be easier to list the ones that don’t do it: hyoscine, dexamethasone, benzodiazepines, cannabinoids, palonosetron (alone among the 5-HT3 antagonists), aprepitant, cyclizine and prochlorperazine (alone among the phenothiazines).
107
Q

Describe the 8 classes of aperients

Clue
- 2 major subclasses of which each has 4 agents

A

4 Aperients
4 laxatives

Aperients
- Bulk
- Soften
- Lubricate
- Osmotic

Laxatives
- Prostaglanding
- Macrolides
- Cholinergic stimulant
- Opioid

108
Q

Bulk forming laxatives include what agents? MOA
Side effects

A

Bulk-forming laxatives
* e.g. Psyllium, Methylcelulose, Polycarbophil
* Large polymers which trap water in a gel matrix, increasing the mass and water content of stool and thus encouraging peristalsis
* Side effects - Abdominal distension (metabolised by gas producing gut bacteria), Bowel obstruction, Delayed absorption of nutrients, Delayed absorption of drugs

109
Q

Osmotic laxatives e/.g/
Work how? Side effects

A

Osmotic laxatives
* e.g. ionic salts (Mg), sugar alcohols (mannitol), saccharides (lactulose), magcogols (polyethylene glycol - macrogol just refers to larger molecular mass PEG 3350)
* Osmotic gradient counteracting colon absorption of water - smaller molecules than large starchy molecules of bulk forming group
* SE - abdominal distension (metabolic substrate for gut bacteria), malabsorption, electrolyte and volume depletion

110
Q

Lubricant laxatives includes? MOA? SE

A
  • Mineral oil - microlax, paraffin
  • Emulsify the stool, increased slipperiness and reduced resistance to passage
  • SE - decreased fat soluble vitamin absorption, pruritis ani, lipid pneumonitis if inhaled
111
Q

Stool softeners include? Action? SE

A

Stool softeners
* Docusate, bisocodyl
* Surfactant effect - increase access of existing water to stool particles increasing its water content reducing its viscocity without causing fluid transit from gut to lumen
* SE - increased absorption of lipids and lipid soluble molecules, more rapid absorption of fat soluble drugs

112
Q

Bowel stimulants include? MOA? SE

A

Bowel stimulants
* Sodium picosulfate, senna
* Increase peristalsis and gut secretory activity by a number of mechanism, including PGE2- mediated increase in chloride secretion and inhibition of enterocyte Na+/K+ ATPase
* SE - enteric neuropathy

113
Q

Macrolide MOA for bowel stimulation? SE?

A

Macrolides
* Act as motilin receptor agonists, which stimulates contraction by activation of smooth muscle L-type calcium channels from gastric antrum through the SB until the ileum, producing increased antral activity, increased gastric emptying, and more high-amplitude propulsive contractions
* Interstingly all macrolides just as effective - so if on azithromycn no need to add erythromycin. Erythromycin however now has little clinical use as an antibiotic with increasing resistance hence utilising it here. It is also used in doses smaller than bacterioinhibitory doses to avoid resistance as there is no selection pressure on bacteria.
* SE
◦ QT interval prolongation
◦ Potential antimicrobial resistance
◦ Increased risk of C. difficile infection
◦ Tachyphylaxis

114
Q

Cholinergic prokinetics action how? SE

A
  • Neostigmine
  • By acting directly or indirectly at muscarinic receptors in the gut (M2 and M3 GPCR) –> DAG and IP3 –>, increase the availability of intracellular calcium and increase the contractility of the intestinal smooth muscle
  • SE
    ◦ Miosis
    ◦ Secretions
    ‣ Salivation
    ‣ Increased bronchial secretions
    ◦ Bradycardia
    ◦ Urinary and faecal incontinence
115
Q

Opioid anatagonsits as bowel stimulants do what?

A
  • Naloxone
  • Reverse peripehral effects of opioids by antagonsim of intestina delta and kappa opioid receptors
  • Theoretically, counter-analgesic effects with systemic absorption
  • May produce peripheral features of opioid withdrawal
116
Q

Lactulose
- Class
- Presentation
- Pharmaceutics
- Mechanism
- Adverse effects
- Duration of action
- Absorption
- Metabolism

A

Primary Pharmacology (11 decks)

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