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35 Cards in this Set
- Front
- Back
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Antiparkinsonian |
levidopa/carbidopa, selegiline, ropinirole |
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Ropinirole |
-Long-acting dopamine receptor agonist -Less likely to produce motor complications and therefore used in patients younger than 60. Risk of motor complications in levodopa is dependent of age of onset PD - Can also be used adjunct with levodopa/dopa decarboxylase inhibitors - Contraindications: - >75 years - Cognitive impairment - Sleep apnea and excessive sedation disorders Side/Adverse Effects - Impulse control disorder, nausea, orthostatic hypotension, hallucinations, increased sleepiness |
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Selegiline |
Monoamine Oxidase Inhibitor Indication: PD alone or with levodopa +/- dopa decarboxylase inhibitors MoA: Inhibits one of the enzymes involved in the metabolism of dopamine and so increases the level of dopamine at the synaptic cleft Side effects: Increase levodopa side effects Drug interaction: avoid any drugs that increase 5HT noradrenaline, and adrenaline` |
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Levodopa |
Class: Precursor to Dopamine Indication: PD MoA: Provides greatest symptomatic benefit and is associated with less freezing, drowsiness, edema, hallucinations and risk of impulse control disorders than dopamine receptor agonist. Side effects: Levodopa induced dyskinesia, On-off phenomenon (motor fluctuations), nausia, orthostatic hypertension, hallucinations Formulations: Levodopa and decarboxylase inhibitor (carbidopa) Patient information: Levodopa absorption for the gut and into the blood brain barriercan be delayed/diminished by protein with a meal |
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Why use a dopa decarboxylase inhibitor with levodopa? |
- Levodopa has low bioavailability when given alone (1-2% gets into the brain) - High levels of dopamine in the gut results in nausea - Dopa decarboxylase inhibitor results in decreased metabolism in the GI tract and decreased metabolism in peripheral tissues - Fewer side effects |
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Long term problems of Levodopa/Dopa decarboxylase inhibitor treatment |
- Motor fluctuations: alternate between on and off periods - Dyskinesia: involuntary muscle movements related to peak dopamine levels - can cause social embarrassment, impaired motor function, injury and weight loss Chorea: hyperkinetic, purposeless dance-like movement Dystonia: sustained abnormal muscle contractions Chronic levodopa response - narrowing of the therapeutic window Long term psychological effects: Delusion/hallucinations = too much activation of dopamine receptors in nuceus accumbens Confusion, nightmares, insomnia Toxic (?) |
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Antiepileptics |
phenytoin, carbamazepine, valproate, lamotrigine |
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Phyenytoin |
MoA: believed to work by inhibiting repetitive firing, by increasing the number of Na+ channels in the inactivated state Indication: All other than absence seizure types Adverse effects: Narrow therapeutic window of plasma concentrations Side effects include: Mild- vertigo, ataxia, headache, nystagmus. Severe - confusion, cognitive dysfunction, hyperplasia of gums, hirsuitism, megaloblastic anaemia, hypersensitivity reactions, hepatitis, lymph node enlargement Can be associated with fetal abnormalities |
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Carbamazepine |
MoA: believed to work by inhibiting repetitive firing, by increasing the number of Na+ channels in the inactivated state Indications: Epilepsy (all other than absence seizures), bipolar, neuropathic pain Common adverse effects: nausea, dizziness, drowsiness, ataxia, rarely - agranulocytosis (bone marrow fails to make enough granulocytes) |
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Valproate |
MoA: inhibit T-type Ca2+ channels in the thalamus, reducing thalamocortical oscillations in absence seizures. Also believed to work by inhibiting repetitive firing, by increasing the number of Na+ channels in the inactivated state. ALso increases GABAnergic inhibition Indications: Epilepsy (All seizure types), bipolar, migraines Common adverse effects: relatively few sedative effects, weight gain, nausea, transient hair loss, bleeding; rarely severe hepatic toxicity |
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Lamotrigine |
Indications: Epilepsy (All seizure types), bipolar disorder, neuropathic pain MoA: believed to work by inhibiting repetitive firing, by increasing the number of Na+ channels in the inactivated state Common adverse effects: blurred vision, dizziness, drowsiness |
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Status epilepticus |
Benzodiazepines MoA: increasing the effect of GABA on GABAa receptors Indication: In status epilepticus (ie continuous seizures for at least 30mins or one seizure following another without recovery), some BZDs are used eg diazepam, clonazepam, lorazepam - given i.v. or i.m. Interactions: other CNS depressants such as alcohol, barbiturates, antihistamines |
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Anaesthetics |
Propofol, lignocaine (local anaesthetic) |
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Antipsychotics |
haloperidol, clozapine, quetiapine, risperidone |
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Haloperidol |
Class: D2 receptor antagonist (magic bullet) MoA: very low activity of the mesolimbic dopamine neurons - no psychosis. very low activity of the nigrostriatial pathway - drug induced parkinsonism Side effects: moderate weight gain, sedation, drug induced parkinsonism, |
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Atypical antipsychotics: clozapine, quentiapine, risperidone |
MoA: Reduced dopamine receptor activation (magic shotgun) - D2 receptor partial agonist - 5HT2a/D2 receptor antagonist - 5HT1a receptor partial agonist What's wrong with clonzapine (used only when other antipsychotics fail even though it has the best efficacy)? - Can reduce psychotic symptoms when other antipsychotics have failed however - Adverse side effects: 0.5-2% develop agranulocytosis (reduction in white blood cells therefore haematological monitoring required), 3% patients develop seizures, constipation can be severe and fatal, myocarditis and cardiomyopathy -Drug interactions: Cigarette smoking - an inducer of CYP1A2 therefore a 50% increase in clozapine levels may occur 2-4 weeks after smoking cessation |
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Antidepressants |
citalopram, fluoxetine, nortriptyline, moclobemide, lithium |
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Nortriptyline |
Class: Tricyclic Antidepressant -Monoamine uptake inhibitor MoA: Blocks reuptake of both 5-HT and NA. Can also block acetylcholine, alpha-adrenoreceptors and histamine receptors. Therapeutic effects: After 2-3 weeks Side effects: Dry mouth, blurred vision, constipation, urinary retention, tachycardia, postural hypotension Overdose: anticholinergic effects cause cardiotoxicity; also confusion and mania Drug interactions: alcohol, anaesthetics, hypotensives, NSAIDs; do not prescribe with MAOIs |
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Moclobemide |
Class: Monoamine Oxidase Inhibitor (MAOI) MoA: Reversible and selective acts on MAOa. Inhibits the enzyme that metabolises mainly 5-HT Side effects: dizziness, insomnia, nausea |
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Monoamine Oxidase (MAO) |
- A widely distributed enzyme that exists in 2 forms, A and B - MAOa is found mainly in the intestinal tract (80% of intestinal MAO), liver, brain and peripheral adrenergic neurons -MAOb is found mainly in the liver and brain - MAOa preferentially acts on serotonin (5-HT) - Inhibition of more than 70% of MAOa activity is necessary for an antidepressant effect - MAOa and MAOb both act on noradrenaline (NA) and dopamine (DA) |
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Citalopram |
Class: Selective Serotonin Reuptake Inhibitor (SSRI) MoA: drugs that preferentially inhibit the reuptake of 5-HT rather than NA thus leaving more serotonin in the synaptic cleft Side effects: nausea, vomiting, diarrhoea, constipation, sexual dysfunction Abrupt discontinuation: 1 in 5 patients, dizziness is the most common symptom |
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Fluoxetine |
Class: SSRI MoA: drugs that preferentially inhibit the reuptake of 5-HT rather than NA thus leaving more serotonin in the synaptic cleft. Fluoxetine still affects NA to some extent Side effects: nausea, vomiting, diarrhoea, constipation, sexual dysfunction Abrupt discontinuation: 1 in 5 patients, |
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Lithium carbonate |
Used prophylactically to treat manic-depressive disorder and sometimes unipolar depression MoA: Still poorly understood, but it is known to block many receptor-mediated effects via depletion of phosphatidyl inositol (PI). Recent evidence that it induces BDNF and blocks NMDA receptors - Narrow therapeutic window with long duration of action; dose monitoring is used -Toxicity: can include cerebellar ataxia, renal failure - Chronic treatment: can lead to mild cognitive deterioration and thyroid disorders -Alternatives to Lithium: Anti-epileptic drugs such as carbamazepine which reduce hyperexcitability by inhibiting voltage-dependent ion channels; can be used in patients who do not respond to lithium |
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Antianxiety/hypnotics |
Diazepam, zopiclone, lorazepam |
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Diazepam, lorazepam |
Class: Benzodiazepines MoA: Increase the effect of GABA on GABAa receptors: they are positive allosteric modulators. They increase inhibition in the CNS, thereby reducing anxiety, although, if the dose increases they will induce hypnosis Side effects: drowsiness, decreased alertness, ataxia Tolerance can develop |
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Zopiclone |
A non-BZD with similar effects |
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Antidiabetic (Hypoglycaemics) |
Insulin, metformin, glicazide, sitagliptin, pioglitazone |
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Metformin |
Preferred initial agent for monotherapy and is a standard part of combination treatments Class: Biguanide Route: Oral Excretion: Tubular renal unchanged MoA: activates hepatic and muscle adenosine monophosphate-activated protein kinase (AMPK), normally activated by AMP accumulation from ATP metabolism (cellular signal for increased energy requirements) -Hepatic AMPK roles: -> inhibits acetyl CoA carboxylase (ACC) to promote FA oxidation -> Decreases expression of transcription factor SREBP-1, implicated in the pathogenesis of insulin resistance, dyslipidaemia, and diabetes -> inhibits hepatic glucose production and promotes increase in skeletal muscle glucose uptake ADRs: DIarrhoea and abdominal discomfort, VitB12 malabsorption, contraindicated in patients with severely impaired renal function, hepatic failure, cardiac failure. Lactic acidosis |
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Glicazide |
Class: Sulphonylureas MoA: stimulate insulin secretion from pancreatic beta-cells -> ineffective if beta-cells destroyed. Mimic indirect action of glucose on ATP sensitive K+ channels. Increase endogenous insulin secretion by: blocking K+ATP channel associated with sulphonylurea receptor on the beta-pancreatic cell. Subsequent membrane depolarisation allowing Ca2+ entry. Ca2+ spike evokes insulin release from islet cells Route: Oral - rapidly absorbed from GI tract. Highly protein bound. Metabolised by liver, metabolites excreted in urine (caution in renal and hepatic insufficiency) ADRs: Hypoglycaemia, weight gain Drug interactions: altered metabolism (alcohol, MAO inhibitors). Altered plasma protein binding (free:bound drug ratios) |
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Sitagliptin |
Class: DPP-IV inhibitor Route: Oral Excreted: In urine (dose adjustments needed in renal failure) Use: As a monotherapy or combination (with metformin or TZDs) in type II DM, or as an adjunct monotherapy to diet and exercise MoA: DPP-IV inhibition results in prolonged activity of incretin hormones (GLP and GIP). THis leads to increased insulin secretion to glucose and decreased glucagon secretion leading to improved glycaemic control. ADRs: respiratory tract infection, nasopharyngitis and headache |
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Incretin hormones |
Incretin effect - Eating promotes release of incretin hormones (insulin secretors) resulting in reduced glucagon -Insulin release greater following oral vs i.v. glucose due to incretin hormone effect Incretin hormones - secreted from ileum in response to glucose (GLP-1 & GIP) - Rapidly metabolised by DPP-IV (a cell surface peptidase -Levels of GLP-1 reduced in patients with diabetes Therapeutic strategy: either -activating GLP-1 using an incretin mimetic or - preventing endogenous GLP-1 breakdown by inhibiting DPP-IV using sitagliptin |
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Insulin |
A range of insulin preparations, individual and premixed currently available Main types of insulin based on duration of action: -very short acting -short acting -intermediate acting (protophane) -very long acting -insulin glargine (24 hr insulin) ADRs: hypoglycaemia, weight gain, lipoatrophy or lipohypertrophy, insulin oedema (renal retention of Na+), transient deterioration in retinopathy, local curaneous allergy or even IgG mediated insulin resistance |
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Antidotes |
Naloxone, flumazenil |
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Naloxone |
-Opioid antidote |
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Flumazenil |
-Benzodiazepine antidote |
