Some of these stimulants are often used/misused by learners and students as cognitive performance enhancers. Do a search on the internet and compile a report on the merits/dangers of this practice.   

During a study where Methylphenidate (MPH), Modafinil & Caffeine were compared to placebos in three different arms; the following results were observed: 

Following the intake of MPH – declarative memory performance was significantly better, an effect that was also shown previously both for the dose of 20mg that was used in the trial and for a higher dose of 40mg (Linssen et al. 2012 & -2014). During the trial, early- as well as late recall was better after intake of the 20mg dosage of MPH. 

However interestingly enough no effects were seen on other cognitive tasks that were applied to test for a variety of cognitive domains – including a test for sustained attention. 

The positive results from the MPH intake are also correlated to studies done with amphetamines. 

The summarized results of the above-mentioned study showed that MPH intake had positive effects on fatigue and long-term declarative memory and caffeine showed positive effects on sustained attention; whereas Modafinil showed no significant effects. According to this study, no negative effects on other cognitive domains were observed. 

Repantis, D., Bovy, L., Ohla, K.  et al.  Cognitive enhancement effects of stimulants: a randomized controlled trial testing methylphenidate, modafinil, and caffeine.  Psychopharmacology 238, 441-451 (2021).  https://doi.org/10.1007/s00213-020-05691-w  

In contradiction – another study by researchers from the University of California, Irvine, states that using stimulants to enhance cognitive performance only bring about short term benefits – but in the long term, these drugs negatively affect focus, working memory, and sleep quality thus creating a “vicious cycle”. 

“Focus boosting drugs not worth the risks, studies warn” ~ Maria Cohut PhD 

https://www.medicalnewstoday.com/articles/326023  

The boost in attention after taking the drug is short-lived: the above-mentioned study compared groups of participants where one group received a placebo, and another group received 20mg of dextroamphetamine, the active ingredient present in Adderall. Results showed that the group who received the stimulant demonstrated improved short term attention than the group who had received the placebo. 75 minutes after receiving the drug, the cognitive performance was 4% better than that of the control group and they also had better focus than they did at baseline. However, at both 12 and 24 hours after taking this drug, participants no longer experienced any benefits. 

“Our research suggests that the purported enhancement to executive function from psychostimulants in healthy populations may be somewhat exaggerated, as we found only minor daytime improvement in attention and no benefit to working memory.” Sara Mednick. 

These stimulants in the long run cause adverse effects on memory and sleep – decreasing the patient’s total sleep time and sleep quality. Another consequence of long-term use is dependence. 

Other long term side effects include: 

• Tachycardia, high blood pressure and possible inflammation of heart valves

• Skin disorders, vitamin deficiency and flushed / pale skin

• Stomach ulcers and malnutrition

• Mental health and behavioural problems 

• Dizziness and difficulty breathing

• Loss of coordination and physical collapse

• Unusual tiredness / weakness

• Repetitive physical actions 

• Convulsions, coma and death 

Even though these stimulants have somewhat beneficial effects on cognitive function – especially short term and thus could improve memory and concentration during exams – misuse of these drugs could quickly deteriorate to dependence and in the long-term negatively affect users’ sleep and cognitive performance. 

Which different groups of hallucinogenic drugs are known? 

1. The arylcyclohexylamine drugs = glutamate NMDA receptor antagonists

   • Phencyclidine (PCP) / aka ‘angel dust’ 

   • Ketamine / aka ‘special K’ 

2. Miscellaneous hallucinogens = 5-HT2A agonists 

   • Lysergic acid diethylamide (LSD) 

   • Mescaline

   • Psilocybin (the active ingredient of ‘shrooms’) 

Hallucinogenic effects can also be seen with Scopolamine and other lipophilic anticholinergic drugs. 

Name a few typical effects of the hallucinogens and discuss the clinical profile of a patient who had taken them: 

PCP is presumably the most dangerous of the hallucinogenic drugs and usually causes psychosis; along with the psychotic reactions, impaired judgement seen with PCP use often leads to reckless & life-threatening behaviours. PCP ought to be classified as a psychotomimetic drug.

The miscellaneous hallucinogens cause effects on the CNS that have been defined as “psychedelic” & “mind-revealing” and they also induce sensory distortion (especially visual = shape and colour distortion). Along with the psychedelic effects, they also cause somatic side effects like nausea, weakness & paraesthesia. These drugs also cause panic reactions and “bad trips” in some people. 

Patient clinical profile: 

PCP & Ketamine: 

• Psychedelic effects lasts roughly 1 hour post-consumption 

• These effects entail impaired memory function, visual alterations and increased blood pressure 

• Unpleasant dreams and vivid hallucinations

• In ↑ doses, these drugs may precipitate unpleasant “out-of-body” and “near-death” experiences 

Miscellaneous:

• Psychoactive effects 30 minutes post-consumption and can last up to 12 hours

• During that period of psychosis-like manifestations, patients appear incapable of making rational judgements and to understand common dangers – leading to increased risks for personal injury or accidents 

How is an overdose of LSD dealt with? 

Pre-hospital care: as in any drug overdose instance emergency medical responders should be contacted with an LSD overdose. In the meantime before they arrive, it is best to reassure & calm the patient down and remove any dangerous / distracting objects or removing the patient from a stressful environment, since sensory overload is a large contributor to “bad trips” experienced in overdose. Sometimes the person needs to be isolated from others to prevent any harmful behaviour – since the real danger of LSD use/overdose is the person’s own actions. 

Medications: Benzodiazepines can be administered to treat agitation, neuroleptic drugs such as haloperidol are not recommended since they may exacerbate psychotomimetic effects. Sometimes massive ingestions of LSD require additional supportive care such as respiratory support and endotracheal intubation; cardiotoxicities are treated symptomatically. 

How is an overdose of anticholinergics dealt with? 

Pre-hospital care involves transporting the patient to the closest ER with advanced life support capabilities, avoid ipecac syrup and ensure that the patient’s airway is open and breathing is present and can be maintained. 

Medical care: provide oxygen to the patient and intubate if severe CNS suppression is present. If the patient is agitated – pharmacological intervention with physostigmine / benzodiazepines can be used. Activated charcoal can be useful for GIT decontamination especially when sustained release anticholinergic agents were used; however usefulness significantly declines more than 1 hour post-ingestion of anticholinergics. 

Medications: pharmacological treatment for overdose of anticholinergic drugs consists of anticonvulsants, antitachydysrhythmics, sodium bicarbonate, physostigmine and sedatives. The recommended physostigmine initial dose for adults is 0.5-1mg by slow IV-push – higher doses can lead to cholinergic toxicity. Wait 15 minutes before re-dosing physostigmine. 

Assignment: you are invited to be a speaker at a meeting of the local Women’s Organisation. The group consists mainly of middle-aged to elderly ladies. 

Topic: “Is it dangerous to use sedatives and sleeping drugs?” 

Reports of statistical research carried out by the CDC (Centers for Disease Control and Prevention) showed results indicating that 4% of American adult citizens use prescription sleeping aids, where the majority of these cases were women between the ages of 50 to 80 years old. 

Additionally, new data released by the Substance Abuse and Mental Health Services Administration provided information indicating that the amount of ER visits regarding overdosing of Zolpidem – an active in some prescription sedatives/hypnotics – nearly doubled between the year of 2005 & 2010, increasing from a number of 21 824 ER cases to 42 274, where 2/3 of those cases were all females. 

What are sleeping drugs? 

According to (Jennifer Casarella, MD); most sleeping pills can be classified as sedative-hypnotic drugs and these drugs’ specific action is to induce and/or maintain sleep. There are different classes of sedative-hypnotics such as benzodiazepines, non-benzodiazepines and barbituates – all with different pharmacological mechanisms of action, but at the end of the day – produce the same desired clinical outcome. 

Why use sleeping pills? 

Physicians often prescribe sleeping pills in order to treat multiple sleep disorders and to generally improve the patient’s quality of sleep. Insomnia is the most popular sleep disorder for which sleeping pills are prescribed. In insomniac patients: the benzodiazepine class of sedative-hypnotics – decreases the time it takes to fall asleep, and/or prolongs the patients total duration of sleep (in the case that the patient sleeps 6 hours or less, sleeping pills do not prolong the normal 8 hours of sleep to for example 10 hours). 

Even though sleeping pills are an effective method of insomnia relief, they are only meant to be used acutely and are not the answer to sleeping problems in the long run! 

“Long-term use of medications for sleep is not associated with reductions in sleep problems,” says Dr Daniel Soloman, a professor of medicine in rheumatology and pharmacoepidemiology at Harvard Medical School and Brigham & Women’s Hospital in Boston. 

What are the potential side effects and risks associated with taking sleeping pills? 

Approximately 80% of sleeping pill users experience the “hangover effect” the following day subsequent to taking sleep medication. This is a phenomenon that causes people to feel drowsy, fuzzy thoughts / muddled thinking, dizziness and balance problems. This effect can seriously impact people’s daily lives since it can impair your ability to drive, go to work and complete other tasks throughout the day. Additionally, as a woman it is not safe to go out and not be in full control of your thoughts and body’s functioning – for various reasons, it is crucial that we women be in full control of our minds and bodies and be able to defend ourselves or escape a potentially dangerous situation. 

Other side effects of taking sleep medication include: 

• GIT problems like constipation / diarrhoea, gas, nausea and heartburn

• Dry mouth

• Headaches

• Muscular weakness

• Changes in appetite

• Daytime drowsiness and possible mental impairment during the day

• Tremors

• Disturbed dreams 

The potential risks and complications of taking sleeping pills: 

The most prominent risk of using sleeping drugs is dependence. When people begin to use sleeping pills for longer than their intended use they increase their risk for developing tolerance. Once tolerance is developed, higher dosages will be required to induce the same effects. Too often people who develop tolerance then start to abuse sleeping drugs and risk addiction. 

Addiction to sleep medication increases the intensity and/or frequency of the normal side effects of the drugs, and can precipitate even worse consequences. This is why it is crucial to stop taking the sleep medication once your prescription expires/ends. 

Other risks of using sleeping drugs are allergic reactions and developing sleep disorders such as parasomnias – which are possibly dangerous behaviours whilst still sleeping, for example sleepwalking. 

Conclusion: 

To conclude by answering the topic question: yes, the use of sleeping drugs / sedatives does entail potential dangers and risks – as is with any drug. When the sleeping medication is used for longer than it is intended is when it starts to become dangerous. If you struggle with insomnia it is always best to consult with your physician, since often simple nondrug therapies are enough to improve sleep. 

Pain:  

Pain is an unpleasant sensory and emotional experience associated with actual/potential tissue damage; and it allows the body to react and prevent further pain. Can be acute/chronic. 

Pain is felt when nerve cells namely Nociceptors detect tissue damage and relay information about that damage along the spinal cord to the brain. Pain can be caused by a variety of stimuli, and the main descriptions of pain are neuropathic, phantom and central pain. Neuropathic is a feeling of electrical shocks & cause tenderness, numbness, tingling and discomfort. Phantom occurs post-amputation of a limb and are painful sensations that feel as if they are coming from the missing limb. Central is described as burning, aching and pressing sensations. 

The brain’s interpretation of pain signals + efficacy of the communication channel between brain and nociceptors dictate how an individual experiences pain. Thus, pain is subjective and levels of intensity differs for everyone. 

The general important principles in pain management can be described by the “pain ladder” designed by the WHO in 1986. This reinforces the basic principle that pain requires assessment, and that if an analgesic is ineffective in pain relief, the prescriber should move one step up the ladder, or referral. 

Classification of drugs used as ADs: 

• MAO inhibitors (MAOIs)

• Tricyclic antidepressants (TCAs) 

• Heterocyclic antidepressants (tetracyclics and unicyclics) 

• 5-HT-NA reuptake inhibitors (SNRIs) 

• 5-HT receptor antagonists 

• Selective 5-HT reuptake inhibitors (SSRIs) 

• Selective NA reuptake inhibitors (NARIs) 

• Circadian rhythm regulators 

What do the existing drugs all have in common regarding their MoA? 

Antidepressants (ADs) relieve depression by potentiation/increase of the NA and/or 5-HT neurotransmitter action within the CNS. Thus, the majority of these drugs ↑ [NA] & [5-HT] at the central synapses, b.m.o: 

• Reuptake inhibition 

• Degradation/metabolism inhibition 

• Antagonism of pre-synaptic alpha-2 receptors 

How long does it take for the AD effects of these drugs to appear? What is the reason for this? 

Even though acute, chemical changes in monoamines in the brain already occur within hours after antidepressant administration, a clinical (anti-depressive) response may only be observed after about 3-5 weeks. This may be attributed to multipotent actions on numerous monoaminergic receptors due to the non-specific increase in 5-HT/NA. 

Recent studies on the matter provide an analogous explanation of why ADs do not provide clinical improvements immediately. The reason provided is that ADs do not target the 5-HT molecule transporters directly, even though multiple ADs (ex some SSRIs) directly bind to 5-HT transporters, this direct binding is not the main underlying MoA. The suggested main MoA is thus that ADs target our DNA – specifically genes that code for 5-HT transporters. ADs ↓ activity of these genes, that then causes less 5-HT molecules to be readily available in the brain for release. There are multiple active 5-HT transporter molecules present in the brain before AD administration, thus it takes a few weeks before this gene suppression gives rise to a noticeable effect on 5-HT within the brain. This is the argued explanation for the delayed clinical response of ADs. 

How do the TADs and the selective serotonin reuptake inhibitors (SSRIs) differ in respect of efficacy, side effects & safety? 

(*Note that both TADs & SSRIs can lead to a serious syndrome called Serotonin syndrome; due to the increase in 5-HT levels. 

What is the action of Mirtazapine? 

Mirtazapine = NaSSA (NA and specific serotonin antidepressant). This drug blocks alpha-2, 5-HT2A and 5-HT3 receptors. Mirtazapine additionally blocks Histamine1 receptors – which may lead to sedation and weight gain; and alpha-1 receptors – which may cause postural hypotension. 

• Mirtazapine causes blockade of the inhibitory alpha-2 R’s, that ↑ both NA (autoreceptors) and 5-HT release (heteroreceptors)

• Indirect stimulation of 5-HT1A – anxiolytic 

• Blockade of 5-HT3 – anxiolytic and anti-emetic 

• Blockade of 5-HT2 – anti-depressive effects 

What is the action of Venlafaxine? 

Venlafaxine = SNRI (Serotonin & Noradrenaline Reuptake Inhibitor). This drug causes moderately selective inhibition of both 5-HT and NA reuptake, more potent selectivity for 5-HT than for NA. Besides for depression, Venlafaxine can also be indicated for use in pain: neuralgia & fibromyalgia, GAD and vasomotor symptoms of menopause. 

What is the action of Agomelatine? 

Agomelatine = circadian rhythm regulator. This drug causes melatonergic (MT1 and MT2) agonism and 5-HT2C antagonism. 5-HT2C receptor antagonism leads to the disinhibition of DA and NA release in frontal cortex of the brain (increase DA & NA release). Agomelatine is indicated for use in Major Depressive Disorder.  

Discuss the possible mechanisms of action of lithium. 

The MoA of lithium salts is mediated by Lithium (Li) ions. The action involves the influence of IP3 and DAG 2nd messenger systems by inhibiting various enzymes which are very important for conversion and re-circulation of membrane phosphoinositides. (IP3 & DAG are essential in monoamine and cholinergic neurotransmission). 

What is the therapeutic index of lithium and what is its clinical significance? 

Lithium has a very narrow therapeutic index of 0.5-1.5 mM. The clinical significance is that lithium can very easily lead to toxicities due to its narrow therapeutic index, thus dosing ought to be done with extreme vigilance and care and the patient’s blood levels must be closely monitored for any toxicity. 

When is lithium used as single drug and in which cases and with which type of drugs is lithium combined? 

Lithium can be used as monotherapy in bipolar disorder, as well as prophylaxis of manic and hypomanic episodes and during the treatment of acute manic episodes. 

Combination therapy: lithium can be used in combination with valproate, carbamazepine, risperidone and haloperidol for psychiatric symptoms. Lithium is also used in combination with clonazepam and lorazepam as mood stabilizers. 

Name 3 clinically significant interactions lithium may have with other drugs. Illustrate your answer with suitable examples of drugs. 

• Dehydration, diuretics (e.g. thiazides), NSAIM’s, ACE I’s & fluoxetine ↑ Li+ levels, toxicity 

• Theophylline, caffeine ↑ renal excretion of Li+ 

• Neurotoxic combination with carbamazepine, Ca2+ blockers, losartan, methyldopa, metronidazole and phenytoin 

• Traditional APD’s worse EPS in combination with Li+ 

Name the major side effects of lithium. 

• Tremors

• Sedation

• Ataxia

• aphasia 

• Muscle weakness, fatigue 

• Polidypsia, poliuria, nocturia 

• Nephrogenic diabetes insipidus (Li+ interferes with kidney’s ability to concentrate urine) 

• Thyroid enlargement 

• Leucocytosis 

• Edema 

• Weight gain 

• Acne, alopecia 

• Sexual dysfunction 

What is the status of the use of lithium during pregnancy and lactation? 

Lithium should only be used in life-threatening emergencies when no other safer drug is available, since lithium has positive evidence of teratogenic effects when used during pregnancy. Lithium use should also be avoided during lactation and can be excreted in the breast milk, causing toxicities in the infant. 

Name 3 other important indications for lithium. 

Major depressive disorder, schizophrenia, used as a mood stabilizer during bipolar disorder and is also used in the treatment of Huntington’s disease. 

Recommendations for Ms B Polar’s case study: 

The adverse effects that Ms B Polar has been experiencing are commonly associated with lithium toxicity – even though her plasma lithium levels are within the therapeutic range (0.5-1.5 mmol/L), the combination of lithium with Indocid may cause these adverse effects. Since lithium and Indocid (a NSAID) cause a toxic drug interaction when administered together. Also the use of a diuretic (“waterpill”) in combination with lithium will decrease the renal clearance of lithium. 

I would suggest cessation of use of the diuretic and NSAID for the patient, or lower the dose of lithium or I would suggest an alternative drug to replace lithium. 

Name an example of each of the 3 phenothiazine sub-families and state how they differ from one another in terms of potency and side effects. 

1. Aliphatic side-chain – Chlorpromazine 

2. Piperidine side-chain – Periciazine 

3. Piperazine side-chain – Fluphenazine 

Chlorpromazine and Periciazine have a low degree of potency and little EPS, whereas Fluphenazine has a higher potency and more EPS. 

Chlorpromazine- and Periciazine’s side effects include:

• Severe sedation

• Anti-cholinergic effects

• Strong alpha-lytic effects (postural hypotension) 

• Cardiotoxicity 

Whereas, Fluphenazine causes less sedation and cardiovascular side effects, and weaker anti-cholinergic side effects & -α-lytic effects. 

Which receptors in particular are blocked by the typical antipsychotic drugs? 

• Mesolimbic D2 receptors

• 5-HT2A receptors

How does the mechanism of action of the atypical drugs differ from that of the typical drugs? 

The typical antipsychotic drugs are multi-potent competitive antagonists that block DA, M, alpha, histamine and 5-HT receptors. Whereas, atypical drugs are multi-potent antagonists that have a higher affinity for 5-HT2 receptors than DA receptors and they have less EPS, prolactin effects and TD. D2 blockers, Clozapine has marked D4 blocking effects and strong M1, H1 and α1-blocking effects. Risperidone and paliperidone increase prolactin as the older drugs do, more EPS as well. 

Which of the receptors blocked by the older drugs reduce the risk of extrapyramidal side effects? 

Dopamine-2 receptors. 

Which of the older drugs have a high incidence of extrapyramidal side effects? What is the reason for this? 

• Haloperidol (a butyrophenone derivative) – due to its potent antagonistic effects on D2 receptors, it has a proven high prevalence of EPS. 

• Piperazine derivatives – due to their high potency they have a strong antagonistic effect on D2 receptors that causes EPS. 

Because of which receptor(s) blockade do the aliphatic group of drugs have a high incidence of autonomic side effects? 

Blockade of alpha-1 receptors and also the blockade of cholinergic receptors (Muscarinic receptors) cause autonomic side effects. 

Which two main groups of drugs are important in the treatment of Parkinsonism?

• Drugs that increase dopamine activity
• Drugs that decrease acetylcholine activity

In what way does Amantadine act as an antiparkinsonism drug?

Amantadine is an antiretroviral drug that has a broad mechanism of action. This drug improves the patient’s rigidity, tremors & bradykinesia – however it is only effective for a few weeks.

MoA = Amantadine is a metaffinoid potentiator of dopamine by means of the following actions:

• Increases the release of dopamine
• Increases the synthesis of DA
• Inhibits the reuptake of DA
• Anticholinergic
• Antiviral
• NMDA antagonist

Discuss the MoA of the antiparkinsonism drugs that indirectly increase dopamine concentration:

• Amantadine (MoA explained above)
• Safinamide = increases DA release and decreases glutamate release.
• Istradefyllin = adenosine A2 antagonist (adenosine inhibits D2 function).
• L-dopa = metabolic precursor of DA, it replenishes the DA stores.
• Selective MAO-B inhibitors = the MAO-B enzyme has a preference for DA as substrate, thus by inhibiting this enzyme, DA won’t be metabolized and thus the concentration of DA in the CNS increases. Examples: Selegiline & Rasagiline.
• COMT-inhibitors = COMT metabolizes l-dopa to 3-O-methyl dopa (3OMD). Increased plasma levels of 3OMD weak therapeutic response with l-dopa (3OMD competes with l-dopa for active transport processes). COMT-inhibitor extend the duration of action of l-dopa, ↓ peripheral metabolism, improved bio availability. Examples: Entacapone.

Which of the dopamine agonists are ergot derivatives and which are not?

• Ergot derivative = Bromocriptine
• Non ergot derivatives = Pramipexole & Ropirinole

List the specific dopamine receptors that are stimulated by each agonist.

• Bromocriptine = potent agonist on the D2 receptors.
• Pramipexole = direct agonist on D3 receptors.
• Ropirinole = D2 agonist

Which of these drugs are classified as neuron protecting drugs? What does this mean?

Selective MAO-B inhibitors such as Selegiline & Rasagiline, as well as Pramipexole.

Neuroprotective therapy means that these drugs slow down the disease progression by preventing neuronal death via intervening in and inhibiting the pathogenic cascade that results in cell dysfunction and eventual death.

In general, these agents reduce oxidative stress, mitochondrial dysfunction, protein aggregation, inflammation, excitotoxicity, cell death, iron accumulation, or neurotrophic factors.

What is the importance of MAO-B selective drugs in the treatment of Parkinsonism?

Monoamine oxidase B is an enzyme that is metabolized in the human body into various chemicals in the brain, including dopamine. Thus by administering medication that blocks the effects of this enzyme – a MAO-B inhibitor – a higher concentration of dopamine is available for use in the brain. This can improve many motor symptoms of PD.

How do the COMT-inhibitors act in Parkinsonism?

COMT metabolizes l-dopa to 3-O-methyl dopa (3OMD). Increased plasma levels of 3OMD weak therapeutic response with l-dopa (3OMD competes with l-dopa for active transport processes). COMT-inhibitor extend the duration of action of  l-dopa, ↓ peripheral metabolism, improved bio availability. Additional drug together with l-dopa, improved response and extended on-time. COMT-inhibitors work in an indirect way.

How does istradephyllin act?

This drug is an adenosine alpha 2 antagonist – thus the concentrations of dopamine will increase (since adenosine inhibits D2 function). Thus if adenosine’s action is inhibited, D2 action won’t be blocked and dopamine will increase.

Discuss the MoA of safinamide?

Safinamide is a novel dual MoA.

• Increases DA
  • potent reversible inhibition of MAO-B
  • Inhibition of DA uptake
• Decreases glutamate release

How does the sensitivity for blockade by a LA compare regarding the following types of fibres:

Myelinated fibres with unmyelinated fibres: the smaller, myelinated fibres have a higher chance and susceptibility for blockade than unmyelinated fibres.

Pressure/touch nerves with the dorsal nerves that transmit pain impulses: activated pain fibres flare much quicker, and pain sensation can be selectively blocked by LA. Fibres in the centre of the large nerve bundle are more slowly blocked than those on the outside of the bundle.

Make a list of the effects of LA on other tissues:

Cardiac tissue:

• Class 1 anti-arrhythmic drugs block Na channels in the cardiac tissues with the purpose of shortening the action potential and to prolong the refractory period.

Skeletal muscle tissue:

• Weak blocking/inhibiting effects, no clinical application

Cocaine:

• “Improves” the state of mind, influences central catecholamine-mediated neurotransmission – thus inhibits NA reuptake.

What is the basis for the selection of a LA?

The selection of the appropriate LA could be based on the clinical indication for the drug, meaning what it is going to be used for. The clinical indication could be one of the following:

• Minor surgical procedures
• Spinal anaesthesia
• Autonomic blockade in ischaemic conditions
• Post-operative analgesia

The selection could also be based on for how long the LA is going to be used for, and also depends on the duration of action of the LA.

Why are LA solutions sometimes saturated with CO2?

Carbon dioxide potentiates the effects of local anaesthetics, meaning it could increase the rate of the LA action.

Which of the LA are typically used for surface anaesthesia?

• Cocaine
• Benzocaine
• Oxybuprocaine

The major effects of the inhalation anaesthetics on every system of the body:   

The major acute toxic effects of inhalation drugs: 

• Nephrotoxicity
• Hematotoxicity
• Hepatotoxicity
• Teratogenic