Stimulants taken by people who do not have the neuropsychiatric condition of ADHD is very dangerous as chronic use my decrease these peoples cognition and may be irreversible to return to their optimal cognitive abilities.

• What different groups of hallucinogenic drugs are known?
  • LSD
  • Psilosibien
  • Mescaline
  • Scopolamine
  • Ketamine
• Name some typical effects of the hallucinogenic drugs and describe the clinical picture of a patient who took them?

Impaired judgment leads to reckless behavior

Mind revealing effects

Also somatic effects nausea, weakness

Panic reactions occasionally relapse

• How to treat an overdose with LSD?

Overdose: Nistagmus, severe hypertension, convulsions, may be fatal.

Treatment after overdose: Flumazenil and even antipsychotics

• How is an overdose of anticholinergics treated?
  • Benzodiazepines for agitation
  • IV fluid in case of hypotension
  • Within 1 hour after overdose: activated carbon

Prepare a short “lecture” of no more than 5 minutes (200 words), in which you have to explain to a client what pain is, what it can cause, why different people experience pain differently and what generally important principles of involves pain management and referral. The above two videos will also be helpful.

pain is described as an unpleasant, subjective sensory and emotional experience associated with actual or potential tissue damage.

According to Johns Hopkins Medicine, pain can be persistent, burning, throbbing, stabbing, pinching or hurting or in many other ways described. Pain can also result in numerous physical symptoms such as nausea and dizziness. Emotional effects such as anger depression can also appear. Pain can occur to such an extent that it affects the person's daily lifestyle, work environment, relationships and dependence.

Johns Hopkins Medicine further elaborates and explains that pain can be classified as acute (severe and short of duration and is usually an indication that the body has sustained an injury) or chronic (ranging from moderate to severe pain and presents for longer periods ).

Pain can be treated in several methods. For moderate pain, non-prescribed medication can be used. Other stronger pain medications and anesthetics may also be used. Some patients may learn to live with pain through distraction, meditation, relaxation, yoga, or cognitive behavioral therapy.

1. Discuss the possible mechanisms of action of lithium.

Lithium ion: Affects cAMP, IP3 and DAG second messenger systems, the latter by lowering several enzymes that are important in the conversion and recycling of membrane phosphinocytes. IP3 and DAG are important in monoamine and cholinergic neurotransmission.

2. What is lithium's therapeutic index and what is its clinical significance?

The therapeutic index is 0.5 - 1.5 mM and anything more than 2 mM can be toxic. It therefore possesses a very narrow or small therapeutic index and can very quickly lead to toxic plasma concentrations. It is therefore important to monitor and monitor blood plasma levels regularly to prevent toxicity due to Lithium.

3. When is lithium used as a single agent and in what cases and with what type of agents is lithium combined?

Lithium is used as a single agent for anti-manic and anti-depressant effects during acute or maintenance phases.

Valproate is used in combination with Lithium for acute manic phase, when the patient does not respond to Lithium.

4. Name 3 clinically significant interactions that lithium may have with other drugs. Illustrate your answer with appropriate drug examples.

• Interactions with diuretics (thiazides), NSAIDs, ACE inhibitors and Fluoxetine increase Lithium levels and may lead to toxicity.
• Interactions with antacids (eg na - bicarbonate), theophylline and caffeine increase renal excretion of lithium in other words decrease the effectiveness of lithium.
• Interactions with Carbamazepine, Calcium channel blockers, Losartan, Methyldopa, Metronidazole and Phenitoin lead to neurotoxicity.
• Interactions with traditional antipsychotics exacerbate extra pyramidal effects in combination with Lithium.

5. Name the most important side effects of lithium.

• Tremore
• Sedation
• Ataxia
• Aphasia
• Muscle weakness
• Fatigue
• Polydipsia
• Polyuria
• Nocturne
• Nephrogenic diabetes insipidus
• Thyroid enlargement
• Leukositoses
• Edema
• Mass increase
• Acne
• Alopecia
• Sexual dysfunction

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

Lithium can lead to lithium toxicity in unborn baby and cause abnormalities such as underdeveloped heart, or affect development of unborn baby's heart.

7. Name 3 other important indications for lithium.

• Anti - depressant
• Schizophrenia
• Mood Stabilizers

8. Evaluate the following case and fully motivate your recommendations:

Ms B. Polar (21 years, 60kg) is a student and has been using the following medication for the past 2 months:

Camcolit 600mg bd. Plasma levels taken after two weeks were 0.8mmol / L. She suffered a muscle injury and has also been using Indocid R® 75mg for the past 10 days. Upon further inquiry, she states that she has "gained an awful lot of weight" and is now simply drinking from her mother's "water pills" in the hope that she can get rid of the extra kilos. However, she complains that she is very tired, struggling to keep her eyes open in class, staying thirsty and constantly shaking and feeling nauseous.

Recommendations:Blood plasma levels fall within the range of the therapeutic index, from 0.5 - 1.5 mmol per liter. My suggestion would be to stop taking the diuretics immediately as it interacts with the Lithium medication. This can lead to an elevated blood plasma level of Lithium which can eventually lead to toxicity. Weight gain is one of the side effects of using Lithium. The non-steroidal anti-inflammatory (NSAIDs) medication, such as Indocid, also interacts with Lithium. It increases blood plasma levels of Lithium and can lead to toxicity. The diuretics therefore increase the excretion of water in the body and her fatigue, nausea, shakiness and dry mouth symptoms can therefore be attributed to it due to some degree of dehydration.

Using your textbooks, compile a classification of the drugs used as antidepressants.

2. With regard to the mechanisms of action of the existing drugs, what do they all have in common?

These drugs have a multiple multipotent action on many monoamine energy receptors and this is due to the nonspecific increase in serotonin or noradrenaline.

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

These drugs have a slow onset of action and take 14 - 21 days or even more before they start working effectively.

4. How do the TADs and the selective serotonin reuptake inhibitors (SSRIs) differ from each other in terms of:

• Effectiveness:TAD requires titration to minimum effective dose while SSRIs can usually start at full dose immediately (NB anxiety).

• Side effects:
  • TAD:
    • Sedation due to H1 receptor blockade
    • Sympathomimetic: tremor, insomnia (decreases NA readmission)
    • Anticholinergics: vision disorders, dry mouth, constipation, urinary retention, confusion (M-block)
    • Cardiovascular: orthostatic hypotension, dysrhythmias
    • Psychoses, precipitate mania
    • Convulsions
  • SSRI:
    • Insomnia, tremor, GIT - disorders, headache, decreased libido, sexual dysfunction, anxiety (acute), EPS (needles, pins, itching, restless legs) withdrawal syndrome
    • The drugs can reduce appetite and overweight patients can thus lose weight.
    • Drugs are not sedative - do not frequent
    • How acute anxiety as toxicity as SSRIs are usually used for it.
    • Initially, there is a sudden increase in the 5-HT levels in the brain that aggravates anxiety, however, it gets better again later.
• Safety
  • TAD overdose:
    • Very dangerous
    • 10 x daily dose can be fatal
    • Agitation, delirium, neuromuscular irritability, convulsions, coma, respiratory depression, circulatory collapse, hyperpirection, dysrhythmias
    • Coma, convulsions, cardiotoxicity
  • SSRI:
    • The drug has a better side effects profile than many other drugs and is safer in acute overdose.
    • May lower appetite and result in weight loss.

5. How does mirtazepine work?

A NaSSA - Noradrenaline and specific serotonin antidepressant.

Blockα2 (blockade of this inhibitory receptor promotes both NA (autoreceptor) and 5 - HT release (heteroreceptor), 5 - HT2A and 5 - HT3. Also blocks H1 and α1. Also indirect stimulation of 5 - HT1A.

6. How does venlafaxine work?

Blocks both 5 - HT and NA readmission, more potent for 5 - HT than for NA.

7. How does agomelatine work?

Restores the body's biorhythms. Primary agonist at melatonin 1 + 2 receptors and an antagonist at 5 - HT2C receptors.

. Name an example of each of the three phenothiazine subfamilies and say how they differ from each other in terms of potency and side effects?

• Aliphatic compounds (such as Chlorpromazine)
  • Low power
  • My extra-pyramidal effects
  • Severe sedation
  • Weight gain
  • Strong anti-cholinergic effects
  • Strong alpha - lithic effects (such as postural hypotension)
  • Cardiotoxics
• Piperidine compounds (such as thioridazine)
  • Low power
  • My extra-pyramidal effects
  • Severe sedation
  • Weight gain
  • Strong anti-cholinergic effects
  • Strong alpha - lithic effects (such as postural hypotension)
  • Cardiotoxics
• Piperazine derivatives (such as flufenacin)
  • High potency
  • More extra - pyramidal effects
  • Weaker anti-cholinergic side effects
  • Weaker alpha - lithic effects
  • Less sedation
  • Less cardiovascular side effects

2. Which receptors are especially blocked by the typical antipsychotic drugs?

These drugs are neuroleptics drugs. The drugs block mesolimbic Dopamine2 receptors. These drugs also have anti-mimetic effects (anti-vomiting) because the Dopamine2 receptors in the CESA are blocked. Dopamine, Muscarinic, Alpha, Histamine and Serotonin receptors are blocked by antipsychotic drugs.

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

MOA for Atypical Remedies:

• Multipotent antagonists (also known as inverse agonists)
• Often higher affinity for 5 - HT2 receptors. Can also block D2.
• Some also: Strong M1 (Closapine and Olansepine), H1 (all) and alpha - 1 blocking effects (Closapine, Risperidone and Ziprasidone)
• Closapine has a pronounced D4 blocking effect, as well as for 5 - HT. But virtually no affinity for D2.
• Ziprasidone is a D2, 5 - HT2A, 5 - HT1D antagonist but a 5 - HT1A agonist.

MOA for typical drugs:

• Multipotent competitive antagonists - block DA2 receptors rather than

5 - HT2 receptors.

• Also blocks: M (Chlorpromazine and Thioridazine), alpha (Fluphenazine the least), H1 (especially Chlorpromazine and the Thioxetene) and 5 HT receptors.

4. Which of the receptors blocked by the older drugs reduces the risk of extrapyramidal side effects?

Dopamine (D2) receptors

5. Which of the older drugs has a high incidence of extrapyramidal effects? What is the reason?

The piperazine derivatives because these drugs have a high potency and therefore tend to have more extra - pyramidal effects.

6. Due to which receptor blockade does the aliphatic group have a high incidence of autonomic side effects?

The alpha - 1 receptor blockade, because it blocks alpha receptors. These side effects include: postural hypotension, ejaculation impotence by CPZ, Droperidol and Chlorpromazine.

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

• Drugs that promote increased dopamine activity.
• Agents that promote reduced anticholinergic activity.

2. How does amantadine act as an antiparkinsonian agent?

Amantadine is an antiviral drug with a broad mechanism of action. It is a metaffinoid potentiator of dopamine. It increases the synthesis and release of dopamine. It also blocks the reuptake of dopamine NMDA antagonist. It only improves rigidity, tremors and bradykinesis and is only effective for a few weeks.

3. Discuss the mechanisms of action of the antiparkinsonian drugs that indirectly increase dopamine concentration.

The mechanism of action of antiparkinsonian drugs that indirectly increase dopamine concentration is explained as follows:

Amantadien:

• Metaffinoid potentiator of DA
• ↑ exemption from DA
• ↑ synthesis of DA
• Block DA re-admission

Selective MAO-B inhibitors:

• MAO B preference for DA as substrate
• ↑ DA concentration in SSS

Safinamide:

• ↑ DA activity

• Inhibition of DA re-admission

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

Bromocriptine = ergot derivative

Pramipexole = not ergot derivative

Ropinirole = not ergot derivative

Rotigotine = not ergot derivative

5. Make a list of the specific dopamine receptors that are stimulated by each agonist.

Bromocriptine: partial agonist at D2 receptors

Pramipexole: affinity for D3 receptor family

Ropinirole: D2 agonist

Rotigotine: D1; D2 and D3 receptors

6. Which of these drugs are classified as neuronal protective drugs? What does it mean?

Substances that can be classified as neuronal protective agents are the MAO inhibitors such as Selegiline and Rasagiline. These drugs therefore increase the dopamine concentration in the central nervous system and suppress the metabolism of dopamine.

7. What is the importance of Monoamine Oxidase B (MAO-B) selective drugs in the treatment of Parkinsonism?

• MAO B preference for DA as substrate
• ↑ DA concentration in SSS
• Neuronutrients, ↓ disease progression
• AI: Pethidine, tramadol, SSRIs, OTC cold preparations, liver dysfunction

8. How do the COMT inhibitors work in Parkinsonism?

• COMT metabolizes l-dopa to 3-O-methyl dopa (3OMD).
• Elevated plasma levels of 3OMD poor therapeutic response with l-dopa (3OMD competes with l-dopa for active transport processes).
• COMT inhibitor prolongs the duration of action of l-dopa, ↓ peripheral metabolism, improved bioavailability.
• Additional drugs with l-dopa, improved response and prolonged on-time.
• Stalevo® Entacapone, l-dopa, carbidopa combination.

9. How does Istradephilin work?

This drug is a selective adenosine A2A receptor antagonist that targets these receptors found in the basal ganglia. This drug stimulates the central nervous system and can show improved motor function. In combination with L-dopa, dopamine activity is increased by this drug by antagonizing adenosine in the basal ganglia.

10. Discuss the mechanism of action of safinamide

This remedy has a dual mechanism of action.

1. Increases dopamine activity. Potent reversible inhibition of MAO-B. Inhibition of dopamine reuptake.

2. Reduce glutamate release.

1. How does the sensitivity to blockade by an LA of the following types of fibers compare with each other?

• Myelinated fibres with unmyelinated fibres.
• Push / bag nerves with the dorsal nerves that conduct pain impulses.

Nerves:

• • Smaller and myelinated fibers more easily blocked than larger and unmyelinated fibers.
  • Activated pain fibers fire faster, pain sensation selectively blocked by local anesthetics.
  • Fibers in the middle of thick nerve bundle block more slowly than those on the outside of the bundle.

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

• Heart:

Class 1 antiarrhythmic drugs (Lidocaine is class 1 drug that blocks Sodium channels in the heart with the aim of shortening the Action Potential and prolonging the refractory period).

• Skeletal muscle:

Weak blocking effect, no clinical application.

• Cocaine:

Increases mood, affects central catecholamine-mediated neurotransmission (inhibits NA reuptake).

3. What is the choice of an LA based on?

The choice of local anesthetics is based on the following factors:

• The type of procedure or operation performed.
• The type of tissue to which the local anesthetic should act.
• The duration of time that these drugs should have a sedative or narcotic effect.

4. Why are LA solutions sometimes saturated with CO2?

Carbon dioxide acts as a buffer for the local anesthetics and therefore it will potentiate the effects of the local anesthetics.

5. Which of the LAs is typically used for surface anesthesia?

• Benzocaine
• Cocaine
• Oxybuprocaine

1. Compile a table for yourself in which you list the most important effects on each system (CVS, CNS, respiration, kidneys, liver and uterus), but also indicate the exceptions. The table is important when it comes to choosing remedies.

2. Name the most important toxic effects of the inhalants.

• Hypoxia
• Hepatotoxicity
• Nephrotoxicity
• Cardiac arrhythmias
• Neurotoxicity
• Respiratory depression / irritation
• Malignant hyperthermia
• Post - operative nausea and vomiting
• Post - operative irritation

 Which antiepileptic drugs affect the metabolism of the Pill (oral contraception) and what are the implications of this? What drugs are safe to give with the Pill?

Phenobarbitone

carbamazepine

Phenytoin

Topiramate

These drugs interfere with the metabolism of oral contraceptives due to protein binding, enzyme induction and enzyme inhibition. Enzyme-inducing antiepileptic drugs interfere with the women using oral contraception and these drugs reduce the effectiveness of contraception and can also lead to increased risk of fetal abnormalities in an unborn baby. Enzymes commonly induced are usually the Cytochrome P450. Carbamazepine also induces its own metabolism and we call it auto-induction.

Remedies that are safe to use with the pill are:

Valproate

Lamotrigine

Gabapentin

Leviteracetam

How is the kinetics of these drugs affected by age (from neonates to the elderly)?

There is individual variation in the absorption and metabolism of these drugs. Most drugs undergo first-order metabolism in the liver and are then in other words unsaturated, which means that as the dose of the drug increases, so can the enzymes involved. With the exception of Phenytoin, which then undergoes saturated metabolism (“zero-order”) at higher doses. Neonates generally undergo slower metabolism. Babies and children undergo faster metabolism than adults, in other words it may seem that the dose for a child is higher than in adults but this is because the metabolism of these drugs takes place faster in infants and children. Elderly people should receive a lower dose because liver and kidney function are no longer optimal.

In which cases is plasma blood level monitoring indicated?

Because some of these drugs have a small therapeutic index, we need to be careful with interactions of other drugs.

Where protein binding occurs, it is essential to monitor these plasma levels. However, there are some drugs that have no effect on the plasma levels in the body (these drugs have a relatively low protein binding capacity) and these include:

Gabapentin

Topiramate

Ethosuximide

Patients who have conditions such as chronic kidney failure, liver disease, hypoalbuminemia, people with burns (due to a lot of plasma lost leading to reduced albumin), pregnancy, malnutrition (not consuming enough protein in diet), displacing drugs (displaced seats of drugs) and age can also affect the amount of plasma proteins