Pharmacology

What are Graded potentials?

From ligand-gated ion channels. Through dendritic branches, summate and vary in size.

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What are action potentials?

From voltage-gated ion channels. From the myelin sheath and neurotransmitters are released from the axons, like acetylcholine.

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What are the millimoles (mM) values for K, Na and Cl inside a resting neurone?

K = 140mV, Na = 10-15 and Cl = 4-30

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What are the millimoles (mM) values for K, Na and Cl outside a resting neurone?

Potassium; K = 4-5mV, sodium; Na = 145mV and Cl = 110mV.

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Why is the resting potential negative?

Leaky potassium channels.

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What is depolarisation?

Na; Sodium enters the cell and K; potassium continues out.

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What is hyperpolarisation?

The K channels remain open or extra K outside the cell.

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What are the four classes of neurotransmitters?

Amines, Amino acids, Peptides and Purines.

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What are the four classes of amines?

Catecholamines, indolquinines, acetylcholine and diamines.

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Name three catecholamines.

Noradrenaline, dopamine and adrenaline.

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Name an indolquinine.

Seretonin.

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Name a diamine.

Histamine.

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Name the three amino acid neurotransmitters?

Glutamate, GABA and glycine.

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Is glutamate inhibitory or excitatory?

Excitatory; an excitatory post synaptic potential; epsp.

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Is GABA inhibitory or excitatory?

Inhibitory; an inhibitory post synaptic potential; ipsp after chloride; Cl- ions enter the neurone through inotropic (ligand-gated ion channels) receptors.

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Is glycine inhibitory or excitatory?

Inhibitory; an inhibitory post synaptic potential; ipsp.

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Name a purine neurotransmitter?

Adenosine triphosphates; atps.

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Draw a retinal ganglion neurone, motor neurone, pyramidal; the cortex and a purkinje; the cerebellum neurone.

c

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Draw Glutamate metabolism.

c

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Draw glutamate.

c.

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Draw GABA metabolism.

c

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Draw GABA.

c.

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What the of neurotransmitter is Serotonin?

An amine; indolamine.

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Draw Serotonin.

C.

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Draw Adrenaline and Noradrenaline.

C.

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Where is Noradrenaline and Adrenaline located.

Locus Coruleus.

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What does VMAT stand for and what does it do.

VMAT; a vesicular monoamine transporter; beta-hydroxylase

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What are MAOs.

MAO; monoamine oxygenases along with COMTs; catechol-o-methyl transferases inactivate and degrade noradrenaline and dopamine.

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Examples of MAOIs; monoamine oxygenate inhibitors.

Antidepressants; such as Rasagiline; Azilect, Selegiline, Isocarboxazid, Phenelzine and Tranylcypromine.

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What is NET and DAT.

The NET; noradrenaline or norepinephrine transporter and the DAT; dopamine transporter.

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What chemicals do neurones release after a noxious stimuli.

1. H+ ions. 2. Bradykinins. 3. Prostaglandins (decreased by NSAIDs; non-steroidal anti-inflammatory drugs or medicines. 4. Potassium ions. 5. ATP.

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What do mast cells release?

1. Histamine. 2. Substance P; which makes the blood vessels more leaky; allows potassium ions and ATP in the extracellular fluid; more action potentials.

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Define Dependence.

A compulsive use of a drug or medicine with addiction and withdrawal symptoms.

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Define Tolerance.

Increased dose for the same effect.

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What is the reward path?

The Mesolimbic Path.

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What type of receptors do opiates, alcohol, nicotine and cannabis act on?

u-receptors; mu receptors; on GABAergic neurones to disinhibit dopamine; found in the nucleus accumbens, from the ventral segmental area

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What is the most common type of headache?

A tension-type headache.

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Symptoms of a tension-type headache.

A pressure and tightness and bilateral localisation.

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What is the treatment; first line and second line fro a tension headache.

1st line; paracetamol and NSAIDs. 2Nd line; aspirin, paracetamol and caffeine.

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Symptoms of cluster headaches.

An abrupt onset of the headache, a continuous excruciating pain, unilateral localisation and the duration is from half an hour to three hours but many per day.

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Symptoms of a migraine.

Throbbing and for the classification of a migraine; the duration is from 4 hours to three days plus one of; associated photophobia and photophobia, associated aura, mostly a unilateral localisation and nausea or vomitting.

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Phases of a migraine.

1. Predominal or aura phase; visual disturbances or a sensitivity to light, smell or noise. 2. The headache. 3. The resolution phase; throbbing and a lack of concentration.

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The acute treatment of migraines.

NSAIDs, analgesics, triptans; 5HT1B/D receptor; R antagonists and anti-emetics like Metoclopromide.

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The prophylaxis of migraines.

Beta-blockers, anti-epileptics, antidepressants and calcium-channel blockers.

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Mood Disorders.

C.

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Define Bipolar 1.

At least one episode of or mania or a mixed episode. A bigger swing from depression with psychosis ad severe depression to mania with psychosis and depression.

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Define Bipolar 2.

At least one major depressive episode with at least one episode of hypomania.

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Define Cyclothymia.

A milder and chronic form of bipolar disorder; lasts at least 2 years; numerous periods with hypomanic and depressive symptoms.

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Name the two types of unipolar disorders.

Major depression and dysthymic disorder.

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Prevalence of depression.

5% in the United Kingdom.

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Name the three tools you can use to diagnose Major Depressive Disorder.

1. PHQ-9 score (out of 27 but intervention at a score of 12 or more). 2. The HADS score ( questions for depression and anxiety and out of 21 but intervention at a score of 10 or more). 3. BDI-II.

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Who created the PHQ-9 questionnaire?

The DSM; diagnostic and statistics manual of the American psychiatric association.

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Summarise the PHQ-9 questionnaire.

1. Little interest ir pleasure in doing things. 2. Feeling down. 3. Insomnia or hypersomnia. 4. Energy. 5. Appetite. 6. Feeling bad about yourself. 7. Concentration. 8. Slow or fidgety. 9. Sucidal.

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What is Dysthymia or Dysthymic disorder.

A persistent depressive disorder; less severe symptoms but lasts longer.

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Whats is the criteria for manic or hypomanic episodes.

An elevated, expansive or irritable mood plus 3 of the following. 1. A goal-directed behaviour. 2. A reduced need for sleep. 3. A self-esteem increase. 4. Spending.

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Duration of mania.

At least a week.

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Duration of hypomania.

At least 4 days; hypomania is less than mania.

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Name the NICE steps for Major Depressive Disorder.

1. Self-help. 2. The Psychological treatment of mood disorders. 3. Medicines. 4. Electroconvulsive therapies; ects.

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Name the types of the psychological treatment of mood disorders; talking therapies.

1. Group based cognitive behavioural therapy; CBT; 12 2-hour sessions over 8 to 12 weeks. 2. Individual CBT; 16-20 sessions in 3 to 4 months. For people with severe depression, two sessions per week might be provided for the first 2 to 3 weeks of tr

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First line and etc for Major Depressive Disorder.

SSRIs; selective-serotonin repute inhibitors; Sertraline, Fluoxetine; Prozac, Paroxetine and Citalopram.

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Name the Noradrenaline or 5-HT; serotonin reuptake inhibitors.

1. SSRIs, NRIs; norepinephrine or noradrenaline reuptak inhibitors; Reboxetine. 3. SNRIs; serotonin-norepinephrine or noradrenaline reuptake inhibitors; dual action; Venlafaxine, Duloxetine and Bupropion. 4. Tricyclics or tricarboxylic acids.

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Name two tricyclics or tricarboxylic acids.

Amitriptyline and Imipromine.

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Name two Atypical Antidepressants.

Trazadone or Mirlazapine.

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Name two MAOIs.

Reversible and selective for maoa; maoi; Moclobemide. Irreversible; Phenelzine.

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Tip for SSRIs.

Must stop SSRIs slowly as a quick drop in serotonin can lead to depression.

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Dispensing notes for antidepressants.

1. Explain that antidepressants should be continued for at least six months following the remission of symptoms, as this greatly reduces the risk of relapses in depression.

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Co-prescribing in Major Depressive Disorder for Anxiety, Agitation or Insomnia.

Short use; less than 2 weeks, a benzodiazepine.

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Co-prescribing in Major Depressive Disorder for Persistent, Severe or Distressing Adverse Effects.

A dose reduction and re-titration or switching antidepressants to an antidepressant less likely to cause that adverse effect.

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Co-prescribing in Major Depressive Disorder for Hyponatraemia.

Onset of hyponatraemia is usually within 30 days of starting the treatment and is not dose linked. E.G. Amitriptyline. Stop the antidepressant, check hydration and can give a sodium solution orally or by IV; intravenous injection or infusion.

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What are the symptoms of Hyponatraemia.

The symptoms of hyponatraemia; a low sodium concentration in the blood. are; dizziness, drowsiness, confusion, nausea and muscle cramps

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When to review someone with depression?

Arrange a review; within one week fro people less than 30 years of age who have been started on an antidepressant. Within 2 weeks for other people.

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Can someone with depression use St John's Wort?

a 50% reduction in the symptoms of depression but insufficient evidence for achieving remission.

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Name three contraindicated medicines or drugs with interaction with St John's Wort.

Oral contraceptives, anticoagulants and anticonvulsants.

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Name three forms of self-help.

1. Self-help leaflets or books, using cognitive behavioural therapy principals. 2. Self-help computer programmes or the internet. 3. Exercise sessions; three each week for up to 1 hour for 10 to 12 weeks.

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Name three types of medications for Bipolar Disorder.

1. Mood stabilising drugs; Lithium; 3 to 4 weeks for start and the plasma concentration monitoring is required. 2. Anticonvulsants; Sodium Valproate or Lamotrigine. 3. Antipsychotics; Risperidone.

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How to treat an acute phase of Mania.

1. A therapeutic trial of an oral antipsychotic; Haloperidol, Olanzapine, Quetiapine, Risperidone or Aripiprazole. 2. If a second-line antipsychotic is not effective, Lithium may be added, or if not suitable, Sodium Valproate may be added instead.

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Four weeks after the acute episode of mania, long-term management of Bipolar Disorder.

1. Continue their current treatment of mania; Haloperidol; an antipsychotic. 2. Start a long-term treatment with lithium to prevent relapses. 3. If Lithium is not effective, Sodium Valproate may be added to the Lithium treatment.

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Is Lithium effective for mania ad depression.

Lithium is effective for mania but not for depression.

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Why else is Lithium good?

An anti-suicidal effect.

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What is effective for depression in Bipolar Disorder.

Lamotrigine and Sodium Valproate for preventing depressive relapses.

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Centrally-Acting Anti-Obesity Agents

C.

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What is the brain path controlling feeding behaviour?

The hypothalamic arcuate nucleus; arc.

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What's Leptin do?

Leptin increases the Insulin sensitivity in the blood by decreasing adiposity and lipotoxicity.

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Name 2 Anti-Obesity drugs or medicines.

Orlistat; Xenical; a triacylglycerol lipase inhibitor and Liroglutide; a GLP-1; a glucagon-like peptide 1 agonist.

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Where is the fear centre in the brain?

The Amygdala.

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Name the NICE steps for Anxiety Disorder.

1. The low-intensity psychological interventions; self-hep approaches. 2. The high-intensity psychological interventions; cognitive behavioural therapy; cbt for social anxiety disorder. 3. Drugs or medicines.

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Name the NICE steps of medicines for Anxiety.

1. SSRIs; selective-seretonin retake inhibitors; Sertraline first. 2. Other SSRIs; Citalopram, Escitalopram, Fluoxetine, Paroxetine; care for withdrawal syndrome and Vilazodone.

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How does GABA; gamma-amino butyric acid bind to GABAa receptors.

GABA binds at orthosteric sites between beta and alpha and opens the chloride; Cl- ion channels.

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How do Benzodiazepines bind to GABAa receptors.

Between the alpha-i and gamma; Y-k or x or y.

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How is Diazepam; Valium excreted? Longer half-life than Lorazepam.

Liver; hepatically as a 2-keto drug so oxidised in the liver. The internet says that Diazepam and its metabolites; including N-desmethyldiazepam; or nordazepam or nordiazepam, temazepam and oxazepam renally; in the urine; glucuronide conjugates.

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How is Lorazepam excreted?

Renally; in the urine at a drug and as a conjugated glucuronide; a 3-OH; hydroxyl drug.

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What is Schizophrenia?

Hallucinations and delusions.

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What are Schizophrenia's positive symptoms?

An increase in abnormal and active behaviours, hallucinations and delusions.

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What are Schizophrenia's negative symptoms?

An absence of normal active behaviours e.g. Inertia.

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What are Schizophrenia's cognitive symptoms?

A disturbance of normal thought processes; e.g. Concentration.

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What class of drug are Antipsychotics?

D2-antagonists.

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How is psychosis caused?

Increased Dopamine.

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Which pathway causes the negative symptoms of Schizophrenia and why?

The Mesocortical pathway; D1 receptors are decreased; from the ventral tegmental area; VTA to the cortex. Involved in the rewards and euphoria.

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Which pathway causes the positive symptoms of Schizophrenia?

The Mesolimbic pathway; D2 receptors are increased; from the VTA to the nucleus accumbens e.g. Inertia..

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Which pathway can cause the side-effect dyskinesia with antipsychotic medicines?

The nigro-striatal path; moves up and down; from the substantial nigra to the basal ganglia.

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What are the two types of antipsychotics?

1. Typicals or First generation antipsychotics. 2. Atypicals or Second generation antipsychotics.

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Examples of first generation antipsychotics.

E.G. Chlorpromazine and Haloperidol.strong D2 antagonism; only for the positive symptoms of Schizophrenia; extrapyramidal side effects and also have strong CYP-450 metabolism; many interactions.

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Examples of low potency antipsychotics.

E.G. Chlorpromazine, chlorprothixene, thioridazine or levomepromazine. More sedating and more anticholinergic; bradycardia and gastrointestinal problems, but have a lower risk of extrapyramidal side-effects.

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Examples of high potency antipsychotics - Preferred.

E.G. Fluphenazine and Haloperidol. Slightly anticholinergic and sedating, but have more weight gain and a higher risk of extrapyramidal side effects.

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Examples of second generation antipsychotics.

E.G. Clozapine, Olanzepine, Risperidone and Aripiprazole. Less extrapyramidal side effects, but metabolic side effects; diabetes and weight gain. Bind to D2 receptors but a high affinity for serotonin; 5HT2A receptors.

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What does 5-HT2A receptors stand for.

5-hydroxytryptamine 2A receptors.

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Clozapine.

Clozapine; a little different from the other atypical. A shorter half-life, why it produces fewer extrapyramidal side effects. However, possible agranulocytosis; fewer granulates in the blood; increased vulnerability to infection; avoid.

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What is epilepsy?

Sudden and excessive high frequency neuronal discharge. Not random but highly synchronous. In the cerebral cortex.

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Summary.

A reduced cortical activity inhibition can lead to epilepsy. An increased cortical activity excitation can lead to epilepsy.

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The two treatment types.

1. Reduced the synaptic excitation; block the glutamate release and the glutamate receptors. 2. Increased the synaptic inhibition; increase the GABA release and potentiate the GABA receptors.

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Is GABA inhibitory or excitatory.

Inhibitory.

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Is glutamate inhibitory r excitatory?

Excitatory.

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Name 4 drugs that block voltage-gated Na+; sodium channels.

E.G. Phenytoin, Carbamazepine, Lamotrigine and Sodium Valproate.

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Name 4 drugs that block voltage-gated Ca+; calcium channels.

E.G. Ethasurimide, Gabapentin, Phenytoin and Pregbalin.

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Name one drug that reduces vesicle fusion.

E.G. Levetiricetam.

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Drugs acting on GABA synapses; Name a drug that increases the GABA levels or concentration and how.

E.G. Vigabatrin and Sodium Valproate. The GABA transaminase inhibitor blocks the GABA breakdown, increasing the GABA levels or concentration and increases the GABA release.

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Drugs acting on GABA synapses; Name a drug that decreases the GABA inactivation.

E.G. Tiagabine. The GABAa tranporter blocks GABA reuptake and increases the GABA in the synaptic cleft.

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Therefore.

An enhanced postsynaptic response; E.G. Benzodiazepines and Barbiturates on the GABAa and the Cl-; chloride ion channels; prolong the channel open out time.

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What kind of molecules cross the Blood-Brain Barrier; CNS; central nervous system molecules.

Small and lipophilic molecules such as glucose and amino acids. No proteins or antibodies; to maintain a biochemical balance.

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Name 2 extracellular enzymes that can block drug absorption.

Peptidase ane Nucleosidases.

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Name 2 intracellular enzymes that can block drug absorption.

Monoamine oxidases; MOAs and Cytochrome P450; CYP450 enzymes.

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Name the 3 membranes of the Meninges.

1. The Dura matter. 2. The Arachnoid matter. 3. The Pia matter.

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What are astrocytes?

The astrocytes from the brain go around the endothelial cells to form a more robust blood-brain barrier. the constituent cells of the blood-brain barrier are; the neuromuscular unit; nvu.

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Name 5 paths molecules can move out of blood capillaries in the central nervous system.

1. A Tight Junction; very important; small, lipophilic or hydrophilic; water-soluble molecules; amino acids. Paracellular diffusion; the intercellular space between the cells e.g. a tight junction or a desmosome.

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What are the Adjusted Lipinski's Rules for the CNS drugs.

1. The LogP; 1.5-2.5. 2. Mr; around 450. 3. Less than 5 Hydrogen; H-bonds. 4. Less than 6 H-bond donors; N; nitrogen-H and O; oxygen-H. 5. Less than 5 H-bond acceptors; N and O. 6. PSA

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Are hydrophilic or lipophilic molecules absorbed more?

Lipophilic molecules are absurd more than hydrophilic molecules but a more than 5 LogP; lipophilic is too low solubility.

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1. Chemical Methods of Drug Delivery to the Brain.

1. Improving peripheral pharmacokinetics e.g. Peptide and Nucleic Acid analogues and protein pegylation; a longer protein so longer to be circulated and absorbed in the blood.

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C.

4. The mimicking transporter substrates e.g. Gabapentin. 5. Inhibiting efflux transporters so the drug is not moved back out. E.G. Can block the P-gp; P-glycoprotein; careful of a toxic accumulation.

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2. Biological Methods of Drug Delivery to the Brain.

1. Nanomedicines; microparticles and nanoparticles. 2. Viral Vectors; ca produce useful monoclonal antibodies and correct genes; administered by injection.

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3. Alternative Methods of Drug Delivery to the Brain; Skipping the Blood-Brain Barrier.

The olfactory epithelium; paracellular diffusion or axonal transport; e.g. The possible peptide delivery to the CNS.

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Name the 4 types of Controlled Drug Release

1. Water penetration-controlled drug delivery systems; Swelling and Osmosis. 2. Diffusion-Controlled drug delivery systems; Reservoir devices and monolithic devices.

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C

3. A Chemically controlled Drug Delivery system; monolithic devices, surface or bulk erosion and pendant systems. 4. Responsive drug delivery Systems; Physical and Chemical.

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Explain the two types of water-penetration controlled devices.

1. Swelling-controlled; HPMC; hydroxymethyl cellulose higher Mr; more hydrogen; H-bonds, higher hydrophilicity; faster water in; re-bond to form a gel matrix; diffuse into the GI tract and blood. E.G. The Geometrix.

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c

Osmotically-controlled; a semi-permeable membrane, an orifice and an osmotic core. The drug is mixed with a water-soluble materiel e.g. NaCl or KCl. water diffuses into the core to form a concentrated solution inside.

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Explain the two types of diffusion-controlled drug delivery systems.

1. A Reservoir Drug delivery System; microporous polymer.Restricted to implantable devices. 2. Monolithic or matrix drug delivery systems; a water insoluble polymer and the drug is dissolved. the drug diffuses out of the matrix.

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Explain the three types of chemically-controlled drug delivers systems.

1. Bulk erosion; most commonly poy(esters), especially poly(lactic acid) and their co-polymers e.g. Poly(lactic-co-glycolic acid). Lactic Acid + Glycolide ----> with waiter; Lactic Acid + Glycolic Acid; natural metabolites so excreted in the pee.

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C.

2. Surface erosion; hydrophobic polymers with very reactive surface groups. E.G. a lactate monomer added for self-catalysed degradation by dropping the pH so an increased release rate of the drug or medicine. Hydrophobic; decreased release rate.

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...A larger surface area of the core; so a faster initial release. A less surface area of the drug core; so a slower initial release.

C.

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Explain Enteric Coatings.

A Chemically-controlled monolithic device. The drug is released as the polymer matrix dissolves. E.G. Enteric coatings; insoluble in the acidic pH in the stomach but dissolves in the small intestines.

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C.

3. Pendant systems; The drug is cleaved onto the polymer backbone with cleavable linkers then the drug comes off the cleavable linkers for release.

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Give an example of three Responsive Delivery systems; Physical and Chemical.

1. Insulin; an acid-labile bond; in a bendromeric system. Uses N; nitrogen; ionises the N groups of the nitrogen drug matrix in an acidic environment like the stomach. The like charges repel so open the structure and releases the drug.

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...At physiological pH normal insulin is insoluble but with glucose oxidase; when glucose is transformed into gluconic acid, the pH drops and insulin becomes soluble.

C.

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2. Enzymatic devices; an amdose coating can be cracked down by bacteria in the GI tract, as known gastrointestinal; GI track; tract bacteria and release a drug or medicine.

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C.

3. Implantable devices; contraception; diffusion-controlled drug delivery system; the coil. The drug or medicine diffuses across a silicone polymer.

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C.

2. Improving lipophilicty e.g. esterification; a reduction of H-bonding; so less cracking and better diffusion. 3. pro-drug approaches e.g. adding Lysine; is recognised by the LAT-1 transporter.

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Is Oral drug absorption fast or slow?

Rapid.

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What does the half-life correspond to in Oral Drug Delivery?

The kinetics of elimination.

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Draw an oral Drug Delivery plasma concentration curve.

C.

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Is Topical dog absorption fast or slow?

Slow.

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What does 'flip flop kinetics' mean?

The absorption is slower than the elimination rate; Topically.

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Advantages of slow absorption.

Absorption is sustained and although a high Cp; concentration of drug in the blood plasma is not achieved, an increased control and a decreased dosing frequency.

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Draw an Topical Drug Delivery plasma concentration curve.

C

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Give 4 disadvantages of Topical drug delivery.

1. Limited to potent drug molecules; less than or equal to 50mg; milligrams. 2. Lipophilic molecules. 3. The area of the patch;

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Problem with a drug with a high melting point?

Less likely to associate with its own molecules; meaning stable so difficult to dissolve in a polymer for transdermal.

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What is the max flux of drug across the skin?

20ug/cm2/hour.

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The Rate In = The Rate Out.

C.

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What is the calculation for transdermal feasibility for a drug requiring a daily dose of drug?

Area(cm2) x J(ug/cm2/hr) = [(1000 x D) / 24](ug/hr)

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What is the barrier for absorption for Oral and Transdermal medicines?

Oral; the gastrointestinal tract. Transdermal; the barrier is; the subcutaneous; SC layer.

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What is the pH like for Oral and Transdermal medicines?

Oral; hostile and variable. Transdermal medicines or drugs; and acidic and lipid barrier.

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How are Oral drugs or medicines and Transdermal medicines help together.

Oral; powders and binders. Transdermal; polymers and solvents.

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What is the duration of delivery for Oral and Transdermal drugs?

Oral; 6 to 18 hours delivery. Transdermal; 0.5 to 7 day delivery.

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What is the rate determining step?

The slowest step in a series of kinetic processes. So, determines the overall rate.

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Give the equation for disposition.

Disposition = Distribution + Elimination.

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Giuv the equation for elimination.

Elimination = excretion + Metabolism; K = Kexc + Kf.

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What are the 3 steps; rate-limiting steps that can give the gradient or slope; K?

1. The dissolution and Drug Release. 2. Absorption. 3. Elimination.

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What is the most usual slowest step and therefore gives the gradient?

The Elimination rate; Linear Kinetics.

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Case A; The Dissolution and Release precesses are the rate-limiting steps.

1. The drugs with poor solubility; dissolution is less than absorption. 2. The modified-release formulations; the release is less than absorption.

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Case B; Absorption rate-controlled kinetics.

K>Kabs Flip-Flop kinetics; Transdermal drug delivery.

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Case B; Absorption rate-controlled kinetics.

The absorption half-life is greater than the elimination half-life. The t1/2abs>t1/2. A considerable amount of drug has not yet been absorbed when the peak; tmax and Cmax is reached. C= B x e-kxt - B x e-kaxt. = logC = logB - (kabs x t) / 2.303.

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Case C; the disposition or the elimination as the rate limiting process

Most common. Kabs>K and the t1/2>t1/2abs. linear kinetics. LogC(the y-axis) = LogB - (kxt(x axis)) / 2.303. The Slope = -k/2.303

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How to know exactly which type f drug delivery it is?

Absolute certainty requires an intravenous; IV bolus infusion to estimate after the elimination rate constant; K or the elimination half-life; t1/2 with no absorption.

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Linear and Non-linear Kinetics.

C.

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Why does non-linearity occur?

Non-Linear kinetics; enzyme saturation occurs at therapeutic concentrations or levels.

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Why does linear kinetics occur?

The saturation of the enzymes and transporters occurs at concentrations much higher than those in the therapeutic range.

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The Medicines design Vertical Theme Lectures.

C.

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Some CNS; central nervous system active compounds; especially narcotics.

Should have an aromatic ring and a basic nitrogen.

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Draw Morphine, Codeine and Heroin.

C.

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Codeine Metabolism.

C.

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Heroin Metabolism.

Heroin -> 6-monoacetylmorphine -> Morphine -> Morphine-3-monoglucuronide -> Morphine-6-glucuronide.

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Why is Buprenorphine a partial agonist?

Agonises the kappa; NOP; nociceptin opioid receptors encoded by the ORL-1; opioid receptor-like-1 gene but reversibly binds with mu; u receptors; so opposes addiction.

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Name the 3 types of opioid receptors in the brain.

1. Mu; u receptors u-opioid peptide; mop receptors; an analgesic, euphoric and addictive effect. 2. Delta receptors; the delta opioid receptor. A GPCR and mood.

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3. The Kappa receptors; kappa-type 3 opioid receptor; a nociceptin opioid peptide receptor; nope; encoded by the OPRL-1 gene; opioid-receptor-like 1 gene; nociception, motor control and mood. Might also have a natural addiction control mechanism.

C.

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How are opioid receptors activated?

Opioid receptors, which are in the bran are activated by endogenous peptides. E.G. Enkephalins, dynorphins and endorphins. These are released by neurones.

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Is Methamphetamine a nervous system stimulant?

The methamphetamine R-isomer; levomethamphetamine was used by Alan baxter; a Scottish Olympic skier used an American nasal decongestant. Levomethamphetamine is a selective norepinephrine releasing agent, no dopamine.

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No euphoria or addiction like that of dextromethamphetamine or the s-isomer or enantiomer of methamphetamine. Not a central nervous system stimulant.

C.

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Draw Amphetamine and Methamphetamine; include the S-isomer and the R-isomer.

C.

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Name the NICE Guideline steps for mild to moderate Analgesia from the Analgesia Ladder.

1. Paracetamol; 1g; gram four times daily. 2. Ibuprofen (400mg TDS); Weak opioid; Codeine; 60mg every 4 to 6 hours; max 240mg daily if NSAIDs are not tolerated. 3. Add Paracetamol; 1g QDS + A low-dose Ibuprofen; 400mg TDS.

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4. Paracetamol + naproxen; 250 mg to 500 mg BD.

5. Weak opioid; Codeine; 60 mg up to four times daily; a max of 240 mg daily in addition to a full-dose paracetamol and/or an NSAID.

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Name 5 types of medicines that can cause depression.

1. Corticosteroids. 2. Oral contraceptives. 3. H2 atomic histamine receptor antagonists; Cimetidine. 4. Calcium-channel blockers. 5. Retinoic acid derivatives; Vitamin A.

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What is the choice of antidepressant for people who are older or can't sleep?

Mirtazepine; less cardiovascular and cholinergic side-effects.

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What is the choice of antidepressant for mood alerting?

SSRIs; selective-serotonin reuptake inhibitors.

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What is the choice of antidepressant in people who have a suicidal risk?

No TCA; tricyclic; tricyclic acid antidepressants.

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What is the choice of antidepressant for people who drink alcohol?

Citalopram or Sertraline.

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How to treat Serotonin Syndrome?

Stop the interacting medicines and Cyproheptadine; a serotonin antagonist.

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What amount of people do not not respond to their first antidepressant?

One third; 1/3.

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What percentage of people don't respond to antidepressant?

20%

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How long for antidepressant withdrawal?

During 4 weeks; e.g. One week on the antidepressant then half a week then a day then a half day.

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