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. 

Attention Deficit Disorder is a behavioural syndrome that results in patients having a short attention span and in many cases learning problems, it is a neuropsychiatric chronic disorder that affect the patients their entire lives. The treatment of the syndrome allows the increased activation in certain important cortical and subcortical areas in the brain which are involved in attention and executive functioning, allowing the patient to function at a certain level of normality to be able to do daily tasks, such as being able to pay attention in class or be able to study for a test. Drugs such as Ritalin and Concerta are often misused by students who do not have this disorder as a study enhancer. However, the use of prescription stimulants without a prescription can be potentially harmful. These drugs work by increasing the concentration of certain neurotransmitters in the brain that control reasoning, problem-solving and other behaviours that can be important for studying and may help many students achieve better results. Studies done using lab rats and administering these drugs at the same capacity as adolescents, have shown changes to the brain chemistry that have an impact on our reward pathway, our locomotor activity, and certain other behaviours as well. These changes have been linked to seriously concerning behaviour such as increased risk-taking, disruptions in the sleep and wake cycle, problematic weight loss. On the other hand, these drugs have also shown anti-anxiety and anti-depressive effects. These stimulants may make it easier for the learner to concentrate, be less fidgety, and gain control over their actions. The student may also fine it easier to focus and listen in school. These types of drugs may also have adverse effects that may be potentially harmful, learners prone to anxiety or agitation, may experience worsening of those symptoms. People with a history of seizures may experience an increased prevalence of seizures. Others experience side effects such as headaches, trouble sleeping, irritability, moodiness, nervousness and in rare cases and increased heartbeat. Stimulant use can be responsible for habit formation, this is due to the quick rise of dopamine after ingesting larger doses which can cause a feeling of euphoria. With regular misuse learners can begin to experience withdrawal symptoms such as depression, fatigue, and sleeping problems. Stimulants like Ritalin may also show effects throughout the body and not just in the central nervous system. In fact, the circulatory, digestive, respiratory, muscular and skeletal, and also the reproductive system can be affected by the use of these stimulants. Without proper use control by a doctor, people can experience very serious adverse effects with non-prescription use. In many cases, without the proper knowledge of these drugs, misuse can be life-threatening.

Brand, L.Prof.  2021.  Study Unit 13: Alzheimer’s Disease, ADD/ADHD, Obesity, Nausea and Vomiting.  Unpublished lecture notes on eFundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation].

Pietrangelo, A. 2019. Effects of Ritalin on the body. Healthline.com. https://www.healthline.com/health/adhd/ritalin-effects-on-body

Wilde, C. 2017. Non-prescription use of Ritalin linked to adverse side effects. UBNow. http://www.buffalo.edu/ubnow/stories/2017/05/thanos-ritalin.html

• Which different groups of hallucinogenic drugs are known?

PCP (Phencyclidine or Phenylcyclohexyl Piperdine)

LSD (Lysergic Acid Diethylamide)

• Name a few typical effects of the hallucinogenic drugs and discuss the clinical profile of a patient who had taken them.

Effects of Hallucinogenic drugs	Clinical profile of patient using Hallucinogens
Blurred vision	Tired and run down
Vomiting	Bloodshot eyes
Weakness	Bad skin tone
Euphoria	Behavioural changes
Dizziness	Lack of energy
Paraesthesia	Poor performance

                      

• How is an over-dose of LSD dealt with?

The administration of anticoagulant drugs, vasodilator drugs, or sympatholytic drugs via intravenous route of administration.

• How is an over-dose of anticholinergic drugs dealt with?

The administration of a reversible acetylcholine inhibitor.

Brand, L.Prof.  2021.  Study Unit 12: Drug dependence.  Unpublished lecture notes on eFundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation].

Katzung, B. G.  2018.  Basic & Clinical Pharmacology.  14^th ed.  California, San Francisco: McGraw-Hill Companies, Inc.

“Alcohol, what really is its effects on my body”

Drinking alcohol increases the activity of the dopamine neurons in the mesolimbic pathways of our brains, which is the reward pathway, alcohol also stimulates the opioid cells that release endorphins. This produces feelings of joy, pleasure, and euphoria. You feel relaxed because the part of your brain that controls the worry and stress is supressed. But the aftermath of alcohol use, especially in excessive amounts is not as pleasant. The cumulative effects of drinking alcohol can lead to the following problems:

• Slurred speech
• Dependence
• Heart damage
• Blackouts
• Liver damage
• Stomach distress
• Infertility, etc.

Alcohol is very rapidly absorbed and distributed throughout the body. The distribution of alcohol depends on the amount of body fluid we have. Women have less body fluids than men, thus a certain amount of drinks may have no effect on a man but may result in a woman becoming intoxicated. In South Africa, the legal limit of alcohol intake is 0.05g per dL, this means that anything more than 2 drinks within an hour will put you over the legal limit. A problem of dependence may start to develop when the intake of alcohol becomes excessive or when more alcohol becomes needed to achieve the same euphoric effects that were experienced with say 2 glasses. This may then be a sign of alcohol dependence which can lead to undesired withdrawal symptoms that make you feel horrible when your blood alcohol concentrations return to normal and the euphoric effects start to wear off.  The help that may be needed to treat dependence problems, depend on the severity of dependence. With moderate dependence, the most important thing is to find a support system that will help and encourage you to stop. By joining a support group, talking to a psychologist or with your parents, it can be managed. When dependence is more severe then other measures such as a rehabilitation centre may be necessary.

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

Sedatives and Hypnotics help to decrease our inhibitions, suppress our anxiety, and produce relaxation. This encourages the continuous use because these drugs enable us to sleep better. Unfortunately, this is not the only mechanism involved with these drugs. Sedatives have been proven to enhance the dopaminergic pathways in our brain which after continuous use, may enhance the development of addiction. These drugs are known as Central Nervous system depressant drugs, excessive use of these drugs can require increased doses due to ineffectiveness and can lead to toxicity or overdose. In many instances this can be fatal. Although the effects that these drugs produce help better our ability to sleep thus allowing us to feel and function better, these drugs are not a permanent solution and should not be used for longer than the recommended time frame.

Brand, L.Prof.  2021.  Study Unit 3. Alcohols. Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation]

Brand, L.Prof.  2021.  Study Unit 12. Drug Dependence. Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation]

Burnett, D. 2016. Drink and be merry: why alcohol makes us feel good, then doesn’t. The Guardian. https://www.theguardian.com/science/brain-flapping/2016/nov/29/drink-and-be-merry-why-alcohol-makes-us-feel-good-then-doesnt

Katzung, B.G., 2018. Basic & Clinical Pharmacology. 14th ed. United States of America: McGraw-Hill Education.

Pietrangelo, A. 2018. The effects of Alcohol on your body. Healthline.com. https://www.healthline.com/health/alcohol/effects-on-body

Pain is an unpleasant or uncomfortable sensation and emotional experience that is associated with actual or potential tissue damage. Pain can be caused by numerous instances, it can due to a specific injury or medical condition. In some cases, the cause of pain may be unknown. Some cause of pain include, stomach aches and cramps, muscle cramps or strains, cuts, burns, bruises, bone fractures, or headaches.  

Different people can experience pain in a different manner, that is the level of pain I feel with a minor injury can differ to the level of pain another person feels with the same injury. This difference in pain experience is due to a few factors such as, there are biological factors that amplify pain signals that are sent to the brain, when nerve fibres are activated repeatedly the brain may decide to become more sensitive to adequately protect the body. Psychological factors also play a role, where nociception and the brain are influenced by a persons emotions, memories and their perception of pain to influence how much pain they experience, environmental factors may also play a role in how we experience pain. Lastly, social factors such as support by family and friends may also influence how we experience pain.

The World Health Organization created a 3-step treatment ladder in the management of pain. The first step is the treatment of mild pain using drugs such as Paracetamol or Ibuprofen. With moderate pain or if the pain has not resolved, the use of weak opioids, such as Tramadol or Codeine, with or without the addition of Paracetamol or Ibuprofen is recommended. Lastly, in the case of severe pain stronger opioids such as Morphine should be considered.  

Anekar, A.A., Cascella, M. 2021. WHO Analgesic Ladder. NCIB. https://www.ncbi.nlm.nih.gov/books/NBK554435/#__NBK554435_dtls__ Date of access: 28/05/2021

Brand, L.Prof.  2021.  Study Unit 11: Opioid Analgesics and Antagonists. Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation]

Erickson, A. 2021. Everything You Need to Know about Pain. Healthline.com. https://www.healthline.com/health/pain Date of access: 28/05/2021

Pate, J.W.  The Mysterious Science of Pain. TedEd. [YouTube video] https://www.ted.com/talks/joshua_w_pate_the_mysterious_science_of_pain/transcript Date of access: 28/05/2021

1. Using your textbooks, draw up a classification of the drugs that are used as antidepressants.

Subclass of Drugs	Examples of Drugs
Tricyclic Antidepressants (TCA’s)	Tertiary Amines: Amitriptyline Imipramine Trimipramine Chlorimipramine Dothiepine Butriptyline Secondary Amines: Nortripyline Desimipramine Lofepramine
Monoamine Oxidase Inhibitors (MAOI’s)	Non-selective: Tranylcypromine MOA-A selective: Moclobemide Other: Isocarboxazid, Phenelzine, Selegiline
Serotonin-norepinephrine Reuptake Inhibitors (SNRI’s)	Venlafaxine Desvenlafaxine Duloxetine
5-HT2 Antagonists	Trazadone Nefazodone
Selective Noradrenaline Reuptake Inhibitors	Reboxetine
Tetracyclic and Unicyclic	Tetracyclic: Mianserin Mirtazepine Unicyclic: Bupropione
Circadian Rhythm Regulator	Valdoxane
Selective Serotonin Reuptake Inhibitors (SSRI’s)	Citalopram Fluoxetine Paroxetine Sertraline

2. What do the existing drugs all have in common regarding their mechanisms of action?

All antidepressants inhibit the reuptake of neurotransmitters through selective receptors thus causing an increase in the concentration of the specific neurotransmitter.

3. How long does it take for the anti-depressive effects of these drugs to appear? What is the reason for this?

It takes 6-8 weeks to achieve optimal effects from the anti-depressant drugs. This is due to the fact that the drug has to build-up its blood level concentrations to a specific level to be able to work effectively.

4. How do the TADs and the selective serotonin reuptake inhibitors (SSRI’s) differ in respect to:

• Efficacy
• Side-effects
• Safety

	Tricyclic Antidepressants	Selective Serotonin Reuptake Inhibitors
Efficacy	These drugs have a higher affinity for reuptake transport receptors than for specific receptors. They are harder to tolerate due to their side effect profile and thus have a lower efficacy.	These drugs are more selective for serotonin transporters, they are much easier to tolerate due to a better side effect profile, thus they have a higher efficacy.
Side-effects	Sedation Anticholinergic: disturbed vision, dry mouth, etc. Orthostatic hypotension Precipitates mania Convulsions Weight gain, sexual disturbances Tremors, insomnia	Insomnia Tremors GIT disturbances Headaches Decreased libido Sexual dysfunction Acute anxiety Extrapyramidal side effects
Safety	When taken at the correct dosage, these drugs are considered safe. But they do have some potentially fatal side-effects and overdose of these drugs can be very dangerous.	Are generally safe for use, but in certain circumstances they may cause problems.

5. What is the action of mirtazapine?

The action of Mirtazepine is the blockade of inhibitory alpha-2 receptors which advances both Noradrenergic receptor activity and Serotonin release. It causes the blockade of Serotonin-3 and 2 receptors and cause the indirect stimulation of Serotonin-1 receptors.

6. What is the action of venlafaxine?

This drug is a SNRI drug which binds to the transporters of both serotonin and noradrenaline reuptake, it is more potent for serotonin receptors. The binding to these receptors presumably causes the enhancement of actions of both neurotransmitters.

7. What is the action of agomelatine?

This drug is an agonist for the Melatonin 1 and 2 receptors which help to regulate the circadian rhythms. It is also an antagonist for Serotonin 2C receptors which helps to improve sleep.

Brand, L.Prof.  2021.  Study Unit 10: Antidepressants. Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation]

Katzung, B.G., 2018. Basic & Clinical Pharmacology. 14th ed. United States of America: McGraw-Hill Education.

• Discuss the possible mechanisms of action of lithium.

The mechanism of action is not well defined. This drug inhibits the action of several enzymes involved in the recycling of neuronal membrane phosphoinositides. This results in the depletion of the second messenger source, PIP2, which will decrease the generation of IP3 and DAG which are important in amine neurotransmission.

 

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

The therapeutic index of Lithium is 0.5-1.5 mM which is very small.

It is used to stabilize the mood swings experienced in patients with Bipolar Disorder.

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

Monotherapy of Lithium is used for Bipolar disorder. Lithium may be combined with Valproate for the treatment of psychiatric symptoms when the patient shows no improvement with monotherapy.

• Name 3 clinically significant interactions lithium may have with other drugs. Illustrate your answer with suitable examples of drugs.
  • Drugs such as diuretics, NSAID’s, ACE inhibitors, and Fluoxetine may increase the Lithium ion levels and can cause toxicity.
  • Theophylline and caffeine can increase the renal excretion of Lithium.
  • Can have neurotoxic effects when used in combination with Carbamazepine, Ca-blockers, Losartan, Methyldopa, Metronidazole, and Phenytoin.

 

• Name the major side effects of lithium.
  • Tremors
  • Sedation
  • Ataxia
  • Aphasia
  • Muscle weakness, fatigue
  • Polidypsia, polyuria, nocturia
  • Nephrogenic diabetes insipidus
  • Thyroid enlargement
  • Leucocytosis
  • Edema
  • Weight gain
  • Acne, alopecia
  • Sexual dysfunction

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

Its use is contraindicated in nursing mothers and the use thereof should be withheld 24-48 hours before delivery. During pregnancy, use of Lithium is thought to increase the incidence of congenital cardiogenic anomalies. The risk for the development of teratogenic effects is low but can contribute to low Apgar scores in neonates.

• Name three other important indications for lithium.
  • Depression
  • Schizophrenia
  • Mania

• Evaluate the following case and fully motivate your recommendations:

Ms B. Polar (21 years, 60 kg) is a student and used the following medication for the past two months:

Camcolith 600mg bd. The plasma levels after two weeks were 0.8mmol/l. She sustained a muscle injury and has been using Indocid® 75mg nocte for the past 10 days. On questioning she reveals that “she had picked up a lot of weight” and is now using some of her mother’s “water pills” in the hope of losing a few of the extra kilos. However, she complains of fatigue, that she has difficulty in keeping her eyes open in class, remains thirsty and constantly feels shaky and nauseous.

Camcolith is a controlled release Lithium Carbonate drug, her plasma levels were 0.8mMol/L which lies within the therapeutic range (0.5-1.5mMol/L). The weight gain is a common side effect that comes with the use of the Lithium tablets. the diuretics (water pills) can cause an interaction with the Lithium tablets which may cause toxicity. The fatigue, constant thirst, nausea and feeling shaky may be due to dehydration caused by the diuretic tablets due to the increased excretion of water. Indocid is a Non-steroidal anti-inflammatory drug, is also known to have an interaction with Lithium tablets which may increase the plasma levels and cause toxicity. Thus, my recommendation would be to stop the Diuretic tablets (water pills), since the Camcolith shows no toxicity, the patient can continue with usage thereof but should be monitored for toxic effects for the duration of the Indocid therapy. Otherwise the patient should be given a different medication to treat her injury.

Brand, L.Prof.  2021.  Study Unit 9:Anti-psychotic Drugs and Lithium.  Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation].

Katzung, B.G.  2018.  Basic & Clinical Pharmacology.  14^th ed.  California, San Francisco: McGraw-Hill Companies, Inc.

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

Aliphatic – example Chlorpromazine

Piperidine – example Periciazine

Piperazine – example Fluphenazine

The aliphatic and piperidine derivatives have the same properties. They have a low potency. Has little extra pyramidal side effects, causes severe sedation. May produce strong anti-cholinergic effects, may cause postural hypotension and can be cardiotoxic.

The piperazine derivative has a higher potency. Has a higher risk for the development of extra pyramidal side effects. Has weaker anti-cholinergic effects and lower chances of causing postural hypotension. Causes less sedation and is less cardiotoxic.

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

The typical anti-psychotic drugs mainly block the mesolimbic Dopamine-2 receptors.

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

The atypical drugs mainly work’s by blocking the Serotonin-2A receptors, instead of blocking the Dopamine-2 receptors while the typical drugs work by blocking the activity of the Dopamine-2 receptors.

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

The blockade of Dopamine-2 receptors reduces the risk of extrapyramidal side effects.

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

Piperazine compounds, due to its high potency and the fact that it has a high affinity for Dopamine-2 receptors.

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

Muscarinic receptors blockade

Brand, L.Prof.  2021.  Study Unit 9: Anti-psychotic Drugs and Lithium.  Unpublished lecture notes on efundi, FKLG 312.  Potchefstroom: NWU.  [PowerPoint presentation].

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

The 2 main groups of drugs that can be used to treat Parkinson’s are

- Drugs that increase dopaminergic activities

- Drugs that decrease cholinergic activities

• In what way does amantadine act as an antiparkinsonism drug?

Amantadine acts as an anti-parkinson’s drug by the following mechanisms:

- This drug is a Metaffinoid potentiater of DA. Thus, it increases DA release, it increases DA synthesis and blocks the reuptake of DA.

- It is a NMDA antagonist that results in anti-dyskinetic effects.

- Amantadine is an Adenosine alpha-2 antagonist. It works as an anti-viral drug that inhibits the D2 receptor function.

Amantadine improves rigidity, tremors, and bradykinesia.

• Discuss the mechanisms of action of the antiparkinsonism drugs that indirectly increase dopamine concentration.

Drugs that indirectly increase the Dopamine concentration do not require enzymatic conversion to an active metabolite. These drugs also do not act directly on the post synaptic dopamine receptors. These drugs also do not have any potentially toxic active metabolites.

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

The ergot derivatives are:

- Pramipexole

- Pergolide

- Bromocriptine

Non-ergot derivatives:

- Ropinirole

- Rotigotine

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

Dopamine 3 = Pramipexole

Dopamine 2 = Ropinirole

Dopamine 1,2 and 3 = Rotigotine

Dopamine 2 = Bromocriptine

Dopamine 1 and 2 = Pergolide

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

MAO-B inhibitors such as Rasagiline and Selegiline are classified as neuro protective drugs. This means that the Dopamine concentration levels in the central nervous system are increased.

• What is the importance of monoamine oxidase B (MAO-B) selective drugs in the treatment of Parkinsonism?

These drugs work with drugs such as Levodopa. MAO-B inhibitors prolong the duration of the effects of Levodopa.

• How do the COMT-inhibitors act in Parkinsonism?

COMT inhibitors metabolize L-dopa to 3-O-methyl dopa (30MD), the increased levels of 3OMD leads to a weak therapeutic response with L-dopa. 30MD competes with L-dopa for active transport processes. These drugs increase the duration of L-dopa thus, decreasing peripheral metabolism and improving bioavailability of the drug.

• How does istradephyline act?

This drug inhibits Dopamine 2 functioning by antagonising adenosine activity preventing the inhibition of dopamine functions. It is an additional therapy to L-dopa or carbidopa therapy that experiences on-off episodes.

• Discuss the MOA of safinamide

Safinamide, increases DA activity, this results in the potent reversible inhibition of MAO-B and results in the inhibition of DA reuptake. This drug also results in the decrease of glutamate release.

Brand, L. 2021. Parkinsonism. Unpublished Lecture notes on eFundi. [PowerPoint Presentation]. Study Unit 8, FKLG 312. Potchefstroom, NWU.

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

(a) myelinated fibres with unmyelinated fibres; and

(b) pressure/touch nerves with the dorsal nerves that transmit pain impulses?

a.  The smaller and myelinated fibers are blocked much easier in comparison to the larger, unmyelinated fibers which are much less sensitive to blockade by the local anesthetics.

b.  Activated pain fibers fire rapidly, thus pain sensation may be selectively blocked by local anesthetics. Fibers that are located in the periphery of nerve thick nerve bundles are blocked sooner than the fibers located in the core of thick nerve bundles. This is because they are exposed too higher concentrations of the anesthetic much earlier.

• Make a list of the effects of LA on other tissues.

Heart: Local anaesthetics have Class I anti-arrhythmic drug effects resulting in cardiac depression

Skeletal muscle: Weak blocking effects, no clinical application.

• What is the basis for the selection of a LA?

A local anaesthetic is chosen due to the following factors:

• • The type of procedure that is being done
  • The type of tissue that the local anaesthetic should be used on
  • The duration of the numbing effect that is needed

• Why are LA solutions sometimes saturated with CO₂?

The Carbon Dioxide acts as a buffer to the Local Anaesthetic. This will potentiate the effects of the local anaesthetic.

• Which of the LA are typically used for surface anaesthesia?
  • Benzocaine
  • Cocaine
  • Oxybuprocaine

Brand, L. 2021. Local Anesthetics. Study Unit 6 [PowerPoint Presentation]. Unpublished Lecture Notes on eFundi. FKLG 312. Potchefstroom:NWU.

• Compile a table, listing the major effects on every system (cardiovascular, CNS, renal, hepatic and uterus) for all the inhalation anaesthetics. This table is important when it comes to the selection of drugs in certain individuals.

Halothane:
Central Nervous system:	Causes fast and smooth induction Increases cerebral blood flow Increases intracranial pressure
Autonomic system:	Causes Bradycardia
Cardiovascular system:	Decreases blood pressure Causes a sensitized myocardium for arythmogenic effects of the catecholamines
Respiratory system:	No saliva, bronchial secretions, or coughing
Musculo-skeletal:	Skeletal muscle relaxing effects Increases action non-depolarization Decreased action depolarization Post-operative shaking due to hypoxia
Uterus:	Decreased muscle contractions External twisting of a baby
Liver:	Hepatotoxic effects (unpredictable and can be very rare)
Enflurane:
Central Nervous system:	Fast, smooth induction convulsions sometimes (not epileptic convulsions)
Cardiovascular system:	No sensitization of the myocardium. Less suppression than Halothane
Respiratory system:	More suppression than Halothane
Isoflurane:
Central Nervous system:	Faster induction Faster recovery than Halothane
Cardiovascular system:	Less suppression than Halothane No sensitization of the myocardium
Respiratory system:	Potent suppression effects
Desflurane:
Central Nervous system:	Even faster induction than Isoflurane Even faster recovery compared to Isoflurane Increased cerebral blood flow and intracranial pressure
Cardiovascular system:	Less suppressing effects compared to Halothane and Enflurane
Respiratory system:	Strong smell that irritates airways When used as an induction drug it may cause coughing, shortness of breath and a laryngospasm
Sevoflurane:
Musculo-skeletal:	Potentiates the effects of the non-depolarising muscle relaxants like the other halogenated ethers.
Has effects similar too Desflurane with less airway irritation
Nitrous Oxide:
Central Nervous system:	Weak anaesthetic effects Potent analgesic effects Amnesia
Cardiovascular system:	No effects
Respiratory system:	Pure Nitrous oxide results in hypoxia Always mix with oxygen or air Recovery phase: fast diffusion from the blood to the alveoli
Musculo-skeletal:	No skeletal muscle relaxation

• Name the major acute toxic effects of the inhalation drugs.

• Hepatotoxicity
• Hypoxia
• Malignant hypothermia
• Nephrotoxicity

Brand, L. 2021. General Anesthetics. Study Unit 5 [PowerPoint Presentation]. Unpublished Lecture Notes on eFundi.  FKLG 312. Potchefstroom:NWU