Pharma List A&B Flashcards

Question

Solifenacin

Answer 1

Muscarinic receptor blocking drugs MOA: - M3 antagonist(Gqàcontraction) Effect: - Relax the muscle in the wall of the bladder

Answer 2

Muscarinic receptor blocking drugs MOA: - Non-selective muscarinic antagonist Effect: - Mydriatic and cycloplegic agent (loss of accommodation)

Answer 3

Muscarinic receptor blocking drugs MOA: - M3 antagonist(Gqàcontraction) Effect: - Bronchodilation

Answer 4

Muscarinic receptor blocking drugs MOA: - M3 antagonist(Gqàcontraction) Effect: - Short-acting (6h) - Decrease detrusor muscle spasms

Answer 5

Catecholamines MOA: (all adrenergic receptors) - Small dose: β-stimulation predominates (HR, SV, CO, PP↑, TPR, BP↓, bronchodilation) - Large dose: α1-stimulation predominates (TPR, BP↑, reflex bradycardia)

Answer 6

Catecholamines MOA: - α1, α2 and β1 agonist Effect: - Vasoconstriction

Answer 7

Catheholimines MOA: - Small dose: D1 à vasodilation, RBF + GFR↑, Na+ excretion↑ - Medium dose: D1, β1 à heart = positive inotropic effect - Large dose: α1 effects à vasoconstriction (TPR, BP↑)

Answer 8

Catecholamines MOA: - β1 agonist Effect: - CO, SV↑

Answer 9

Catheholimines MOA: - Non-selective β-agonist Effect: - Positive inotropic and chronotropic effect via β1 - Bronchodilation via β2

Answer 10

Indirect symoathomimetic MOA: - Indirect sympathomimetic + weak β2 agonist Effect: - Enhance monoamine release

Answer 11

Indirect symphatomimetic alpha 1 agonist MOA: - α1-agonist Effect: - Vasoconstriction (increased BP, duration of action: 15-60 min)

Answer 12

Indirect sympathomimetics. Selective and α-2-agonists MOA: - α2-agonist (act as sympatholytic) + I2-agonist (imidazole) Effect: - Presynaptic α2 leads to decrease in release of NEàdecrease in BP

Answer 13

Indirect sympathomimetics. Selective and α-2-agonists MOA: - α2-agonist (+ I2-agonist) Effect: - Vasodilation

Answer 14

Indirect sympathomimetics. Selective and α-2-agonists MOA: - α2-agonist Effect: - Inhibit NE release via presynaptic α2-receptor (cannot activate adrenergic receptors àsafe in pregnancy)p Indirect sympathomimetics.

Answer 15

Indirect sympathomimetics. Selective α-1 and α-2-agonists MOA: - Local α1-agonist - Systemic α2-agonist (exception in effect from the sympatholytic effect of α2-agonists) Effect: - Vasoconstriction (local use)

Answer 16

Indirect sympathomimetics. Selective α-1 and α-2-agonists MOA: - α2-agonist Effect: - Inhibit NE release via presynaptic α2-receptor (cannot activate adrenergic receptors àsafe in pregnancy)

Answer 17

α-receptor antagonists MOA: - α1-selective antagonist Effect: - Relax muscle of prostate + bladder neck allowing urine to flow more easily

Answer 18

α-receptor antagonists MOA: - Non-selective α-antagonist (reversible competitive) Effect: - Vasodilation, lower BP

Answer 19

Alpha receptor antagonist MOA: - α1-selective antagonist, β-antagonist Indication: - Hypertension, CHF, chronic stable angina

Answer 20

Alpha receptor antagonist MOA: - α1-selective antagonist, α2-agonist - Serotonergic agonist, β-antagonist

Answer 21

Non-selective β-antagonist MOA: - Non-selective β-antagonist Effect: - HR↓àdiastolic perfusion↑àO2 demand↓

Answer 22

β1-selective antagonists: MOA: - α1-antagonist, β-antagonist

Answer 23

Non-selective β-antagonist MOA: - Non-selective β-antagonist Effect: - Decreased aqueous humor secretion

Answer 24

Non-selective β-antagonist MOA: - Non-selective β-antagonist + (K+-channel blocker) Effect: - Decreases HR + AV conduction

Answer 25

β1-selective antagonists: Metoprolol: (2x 25-100mg) MOA: - β1-selective antagonist Effect: - Local anesthetic effect (inhibit Na+-channels)

Answer 26

β1-selective antagonists: MOA: - β1-selective antagonist Indication: - Hypertension, chronic stable angina, CHF

Answer 27

β1-selective antagonist MOA: - β1-selective antagonist Effect: - NO-dependent vasodilation – better for young males

Answer 28

β1-selective antagonists MOA: - β1-selective antagonist Effect: - Ultrashort effect (ca. 9 min)

Answer 29

Spasmolytic agents MOA: - GABAB receptor agonist Effect: - GiàK+-effluxàhyperpolarizationàlong-lasting muscle relaxant effect

Answer 30

Spasmolytic agents: MOA: - Unknown mechanism (may involve inhibition of Na+ and Ca2+-channels) Effect: - Reduction of muscle reflex

Answer 31

BDZ Spasmolytic agents: Diazepam: (benzodiazepine) MOA: - GABAA receptor agonist Effect: - Cl- influxàhyperpolarizationàmuscle relaxant effect

Answer 32

Spasmolytic agents: MOA: - α2 agonist Effect: Pre-synaptic stimulationàinhibition of glutamate releaseàmuscle relaxation

Answer 33

Direct-acting muscle relaxants: MOA: - Ryanodine receptor (RyR) antagonist Effect: - Inhibits Ca2+ release in ER in the skeletal muscleàreduce actin-myosin interaction

Answer 34

Choliergic antagonist Non-depolarizing agents MOA: - Competitive antagonist of NM ACh-R Effect: - Bind to receptor instead of AChàno opening of ion channelàmuscle paralysis

Answer 35

Non-depolarizing agents MOA: - Competitive antagonist of NM ACh-R Effect: muscle paralysis

Answer 36

Neuromuscular junctiona blocker Non-depolarizing agents MOA: - Competitive antagonist of NM ACh-R Effect: - Bind to receptor instead of AChàno opening of ion channelàmuscle paralysisk

Answer 37

neuromuscular junction blocker nondepolorazing agents MOA: - Competitive antagonist of NM ACh-R Effect: - Bind to receptor instead of AChàno opening of ion channelàmuscle paralysis

Answer 38

MOA: - Selective agonist of NM receptor (depolarizing) Effect: - Skeletal muscle relaxant - Provides depolarizing blockade that cannot be antagonized by ACh-esterase inhibitors (phase 1 blockade)

Answer 39

Local anaesthetic Esters: MOA: - Na+-channel blocker Effect: - Blocks NE re-uptake into nerve terminals (àvasoconstriction + psychostimulant) • Intrinsic sympathomimetic effect

Answer 40

Local anaesthetics Amides MOA: - Na+-channel blocker Effect: - Decreased Na+-influxàraise depolarization thresholdàno membrane depolarizationàblock formation of APàblock generation + conduction of nerve impulses Bupivacaine - local surgical procedure

Answer 41

Local anaesthetics Esters MOA: - Na+-channel blocker Effect: - Reversibly stabilizes the neuronal membraneàdecreases its permeability to Na+- ionsàdepolarization of neuronal membrane inhibitedàblocking the initiation + conduction of nerve impulses

Answer 42

Natural opioids MOA: - Na+-channel blocker Effect: - Reversibly stabilizes the neuronal membraneàdecreases its permeability to Na+- ionsàdepolarization of neuronal membrane inhibitedàblocking the initiation + conduction of nerve impulses

Answer 43

Natural opioids MOA: - Weak agonist (MOR) + natural - Centrally acting antitussiveàdecreases sensibility of cough centers Effect: - Antitussive (suppress cough reflex) - Weak analgesic effect in combination with NSAIDs or acetaminophen

Answer 44

Opioids semi- synthetic Strong agonists: - Semi-synthetic strong agonist - 8x more potent than morphine – pharmacological effects similar to morphine - Oral administration (fast absorbing tablets)

Answer 45

opioids Semisynthetic weak agonist - Codeine derivative à more potent than codeine - Antitussive effect, stronger analgesic effect than codeine

Answer 46

Opioid Semi-synthetic strong agonist (potential drug of abuse!) - Codeine derivative - Similar to morphine – used in cancer associated pain + chronic musculoskeletal pain

Answer 47

Opioids Mixed agonist-antagonists: - Partial μ agonist + κ antagonist (semisynthetic) - 20x more potent than morphine (àresistant against naloxone) - Indication: analgesia, respiratory depression

Answer 48

Opioids Mixed agonist- antagonist - μ antagonist + κ agonist (semisynthetic) - Indication: spinal anesthesia (given after cesarean section as it does not relax uterus) - Effect: • ‘’Ceiling effect’’: respiratory depression will reach a limit, where increasing the dose will not increase the depression • Fewer cardiovascular effects • Naloxone antagonism is weaker

Answer 49

Opioids Strong agonist Meperidine: (pethidine) - Synthetic strong agonist - Shorter duration of action (2-4h) than morphine - Indication: analgesic use (emergency ca

Answer 50

Opioids - Synthetic strong agonist - Similar to morphine à 100x more potent - Short acting

Answer 51

Opioids Synthetic strong agonist - Indication: • Management of opioid withdrawal syndrome • Maintenance programs for addicts (heroin, morphine) - Longer duration than morphine + good oral bioavailability

Answer 52

Opioid Synthetic weak agonist - Inhibitor of NE + 5-HT re-uptake - Used in case of neuropathic pain

Answer 53

opioid agonist Synthetic weak agonists - Anti-diarrheal agents à ↓GI motility + secretions - Loperamide penetrates BBB with difficulty à no CNS effects

Answer 54

Opioids Pure antagonist - Semisynthetic strong antagonist - Antagonist on all opioid receptors (highest affinity to μ receptors) - Short-acting, given IV/IM – oral naloxone together with oxycodone - Indication: management of acute opioid overdose (IV only)

Answer 55

zperipheral μ-opioid antagonist Pure antagonist - Peripherally acting antagonist (cannot penetrate BBB) - For the treatment of opioid induced constipation – if other laxatives are ineffective

Answer 56

NSAIDS Cox inhibitor MOA: - Inhibition of platelet aggregation Effect: - Irreversible inhibition of COX enzyme in plateletsà↓thromboxane A2à↓effect of platelet aggregation

Answer 57

Management of acute gout attacks: MOA: - Microtubule assembly inhibitor Effect: - Binds to tubulin à prevents polymerization, inhibits migration of leukocytes + phagocytosis, inhibits release of lysosomal enzymes - Tubulin is necessary for normal cell division, motility etc. à mitosis inhibitor

Answer 58

-Managment of chronic gout MOA: - Uric acid synthesis inhibitor Effect: - Inhibits the enzyme (xanthine oxidase) responsible for the production of uric acidà ↓ serum uric acid

Answer 59

Managment of chronic gout MOA: - Recombinant urate oxidase Effect: - Urate oxidase enzyme catalyzes the metabolism of uric acid to allantoinà↓serum uric acid, ↓uric acid preparation

Answer 60

NSAIDs -Excellent analgesic effect, weak anti-inflammatory drug - Its use has decreased in many countries because of BM toxicityàagranulocytosis

Answer 61

NSAIDs Analgesic use + moderate anti-inflammatory action - Management of dysmenorrhea à menstrual cramps (uterine relaxation) - Acts for more than 12 hours

Answer 62

NSAIDs Non-selective COX inhibitor - Analgesic use in children (safer than aspirin) - Used to induce ductus arteriosus closure

Answer 63

NSAIDs Strong anti-inflammatory drug, but significant toxicity - BM toxic effect - Gout, arthritis

Answer 64

NSAIDs Short acting, strong anti-inflammatory drug - Indication: acute gout attacks, ductus arteriosus closure, BM suppression

Answer 65

NSAIDs Strong anti-inflammatory drug - Indication: chronic rheumatic pain (accumulates in synovial fluid) à joints

Answer 66

Nsaids Non-opioid analgesic MOA: - Popular analgesic + antipyretic drug - No anti-inflammatory or antiplatelet effect Effect: - Inhibition of COX in the CNS Indication: - Analgesic and antipyretic agent - Aspirin substitute à in children with viral infection or those with aspirin hypersensitivity (can also be used in pregnant women)

Answer 67

NSAIDs COX-2 > COX-1 - Anti-inflammatory

Answer 68

NSAIDs MOA: - COX-2 selective (reversible) inhibitor - Not more effective than the non-selective COX inhibitor) Effect: - Analgesic, antipyretic, anti-inflammatory

Answer 69

Drugs for headache symptoms MOA: - Selective 5-HT1D/1B agonist Effect: - Vasoconstriction of meningeal vessels, prevent release of vasoactive peptides, inhibit pain pathway

Answer 70

Migraine prophylactic therapy MOA: - CGRP antagonist (calcitonin gene-related peptide receptor) Effect: - Decrease inflammation in meninges caused by CGRP

Answer 71

Migraine prophylaxis therapy MOA: - Ca2+-channel blocker, anti-histamine Effect: - Reduce neurogenic inflammation, promote cerebral perfusion

Answer 72

Migraine prophylactic therapy MOA: - Non-selective β-antagonist Effect: - HR↓àdiastolic perfusion↑àO2 demand↓

Answer 73

Migraine prophylactic therapy MOA: - Cardioselective Ca2+-channel blocker Effect: - Slower conduction by SA and AV nodes (Ca2+-dependent cells)à↓HR

Answer 74

Migraine prophylactic therapy Effect: - Facilitate inhibitory actions of GABA Indication: - Antiepileptic

Answer 75

Tricyclic antidepressants (TCAs) inhibit the NE and 5-HT reuptake transporters (NET + SERT) - Action: • Elevate mood, improve mental alertness, increase physical activity

Answer 76

Gas Weak general anesthetic on its own (weakest among all inhaled anesthetics)à cannot produce surgical anesthesia, but has analgesic effect

Answer 77

inhaled anaesthetic Volatile liquid Isomer of Enflurane - Irritates respiratory system (pungent) à only suitable for maintenancec

Answer 78

Inhalerional anasthetic Volatile liquids Rapid onset + recovery - Irritates respiratory system (pungent) à only suitable for maintenance

Answer 79

Inhalationall anasthetics Volatile liquid Most commonly used inhaled anesthetic (potent) - Rapid onset + recovery (à rapidly eliminated) - Less irritation to respiratory system than the othersàused as anesthesia in childre

Answer 80

Barbiturate (IV anaesthetic) Mechanisms: - Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx Indication: - Induction of anesthesia - Anesthesia for short surgical procedures

Answer 81

IV anaesthetic Mechanisms: - Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx - Causes decreased level of consciousness and amnesia Indication: - Induction and maintenance of anesthesia - Outpatient anesthesia - Antiemetic effect (treat postoperative vomiting and nausea)

Answer 82

IV anaesthetic Mechanisms: - Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx Indication: - Only for induction of anesthesia in patients with limited cardiac or respiratory reserve (e.g. hypovolemic patients)

Answer 83

IV anaesthetic Mechanisms: - NMDA receptor (glutamate) antagonist - Produces ‘’dissociative anesthesia’’ à patient remains conscious but has marked analgesia, amnesia and catatonia (lack of movement + communication) Indication: - Induction of anesthesia only for short interventions (e.g. pediatrics, gynecology, burn patients that have to change bandages several times a day)

Answer 84

IV anaesthetic.Benzodiazepines Mechanisms: - Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx Indication: - Not real anesthetic à effect is not narcosis, but deep sleep - Preoperative sedation - Induction of anesthesia

Answer 85

IV anaesthetic Mechanisms: - α2 agonist Indication: - Short-term sedation in ICU settings - Hypertension, as it decreases BP

Answer 86

Opioid IV. Anaesthetic Mechanisms: - Opioid μ-receptor agonist - Analgesic agent Indication: - Induction and maintenance of anesthesia

Answer 87

Preoperative medication Antiemetic

Answer 88

Parasympatolitic Mechanism: - Non-selective muscarinic antagonistàdecreases PARA tone Indication: - Reduce salivation and bronchial secretions before surgery - Decrease of increased vagal tone due to administration of inhaled nar

Answer 89

IV anaesthetic

Answer 90

IV anaesthetic

Answer 91

IV anaesthetic

Answer 92

Benzodiazepines MOA: - GABAA receptor agonist Effect: - Cl- influxàhyperpolarizationàmuscle relaxant effect

Answer 93

Benzodiazepines MOA: - GABA receptor agonist Indication: - Sleep disorders, insomnia Extra: - Short-acting - Hepatic metabolism

Answer 94

Benzodiazepines MOA: - GABA receptor agonist Indication: - Anesthesia (IV), preoperative sedation Extra: - Ultra-short-acting - Hepatic metabolism

Answer 95

Benzodiazepines MOA: - GABA receptor agonist Effect: - Cl- influxàhyperpolarizationàmuscle relaxant effect Indication: - Anxiety, panic attacks and phobic disorders

Answer 96

Benzodiazepines MOA: - GABA receptor agonist Effect: - Cl- influxàhyperpolarizationàmuscle relaxant effect

Answer 97

Benzodiazepines GABA antagonist (at BDZ binding site on GABAA receptor) - Rapid onset, short duration - Reverses effect of BDZs in sedation/anesthesia + overdose of benzodiazepines

Answer 98

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics MOA: - GABAA agonistàhigh affinity to BDZ receptors with α1 subunits Indication: - Sleep disorders (especially sleep-onset insomnia)

Answer 99

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics MOA: - Non-GABAergic hypnotic - Ramelteon = MT1 + MT2 agonists Effect: - Melatonin receptors have important roles in the regulation of the sleep-wake cycle (suprachiasmatic nucleus) - Decrease time of sleep onset during chronic insomnia à no rebound insomnia

Answer 100

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics MOA: - Non-GABAergic anxiolytic - 5-TH1A partial agonist (agonist on its own, antagonist together with full agonist) Indication: - Generalized anxiety disorderso

Answer 101

Butyrophenons (1st generation (“typical”) antipsychotic agents ) Mechanism: - Most widely used typical antipsychotic agentàhigh potency (D2 >> M, α1) - Makes the patient calm and detached from the environment Indication: - Management of acute psychotic disordersàacute delirium

Answer 102

Butyrophenons (1st generation (“typical”) antipsychotic agents) D2 > α1, H1 - Has sedative effectàused in neuroleptanalgesia (together with fentanyl)

Answer 103

Antipsychotic 2nd generation Mechanism: - High affinity for 5-HT2A, muscarinic and adrenergic receptors (antagonists!) - Weak D2 antagonist - No tardive dyskinesia Indication: - Schizophrenic patients resistant to 1st generation antipsychotics

Answer 104

Antipsychotic 2nd generation Mechanism: - 5-HT2AC > D2, M, H1, α1 à improves negative symptoms Indication: - First drug of choice in schizophrenia (most sedative drug) - Also proven to be anti-maniac and have mood stabilizing effect

Answer 105

2nd generation antipsychotic Mechanism: - D2 > 5-HT2A receptor antagonist (but has good affinity for both) Indication: - Schizophrenia (most sedative drug together with olanzapine) - Bipolar disorders

Answer 106

2nd generation antipsychotic Mechanism: - 5-HT2AC > D2, H1, α1 à improves negative symptoms Indication: - First drug of choice in schizophrenia - Tics of Tourette disorder in children

Answer 107

2nd generation antipsychotic Atypical antipsychotic, D2/D3 antagonistàused in management of alcohol psychosis

Answer 108

2nd generation antipsychotic Mechanism: - 5-HT2Aàimproves negative symptoms - Partial D2 agonist Indication: - Schizophrenia - Bipolar disorder (long-acting, T1/2 up to 3 day

Answer 109

2nd generation antipsychotic Atypical antipsychotic, D2/D3 antagonistàschizophrenia, bipolar disorder (Hungarian development)

Answer 110

Antidepressant Tricyclic antidepressants (TCAs) inhibit the NE and 5-HT reuptake transporters (NET + SERT) - Action: • Elevate mood, improve mental alertness, increase physical activity - Uses: • Major depression, phobia/panic anxiety, neuropathic pain, migraine,

Answer 111

MAO INHIBITOR Antidepressants MOA: - Selective and reversible MAO-A inhibitor Effect: - Increased NEàhypertensive crisis (TCAs) - Symptoms: increased BP, arrhythmias, hyperthermia, excitation

Answer 112

Antidepressants Selective serotonin reuptake inhibitors First line therapy against depression à GOLD STANDARD! - Indication: • Depression à 2 weeks to show improved mood (4-6w for max benefit) • Other: generalized anxiety disorder, OCD, PTSD, bulimia • Contraindication: pregnancy - Effect: • Selective inhibition of 5-HT reuptake • Little blocking activity at M, H1, α1 receptorsàless side effects

Answer 113

Selective serotonin reuptake inhibitors First line therapy against depression à GOLD STANDARD! - Indication: • Depression à 2 weeks to show improved mood (4-6w for max benefit) • Other: generalized anxiety disorder, OCD, PTSD, bulimia • Contraindication: pregnancy - Effect: • Selective inhibition of 5-HT reuptake • Little blocking activity at M, H1, α1 receptorsàless side effects

Answer 114

Selective serotonin and NE reuptake inhibitors Selective inhibition of 5-HT + NE reuptake - Used to treat patients that do not respond to SSRIs - Little blocking activity at M, H1, α1 receptors à less side effects

Answer 115

Selective NE reuptake inhibitor Selective NE reuptake inhibitor - Increases mental alertness, motivations, activity - Side effects: dry mouth, hypertension, constipation

Answer 116

Norepinephrine and serotonin receptor antagonist antidepressants. MOA: - α2 selective antagonist (presynaptic) - 5-HT2A/C, 5-HT3, H1 receptor inhibition Effect: - Increased NE synthesis + release à weight gain - 5-HT2C inhibition: stimulation of DA + NE pathways à anxiolytic effect - 5-HT3 inhibition: lack of nausea, vomiting and diarrhea à antiemetic - H1 inhibition: sedative

Answer 117

Norepinephrine and serotonin receptor antagonist antidepressants. MOA: - Melatonin (MT1 + MT2) agonist - 5-HT2C antagonist Effect: - Recovery of circadian rhythm - Better sleep and sexual function

Answer 118

Norepinephrine and serotonin receptor antagonist antidepressants Indication: - Acute treatment of bipolar disorders (manic-depressive diseases) - Maintenance therapy à decrease frequency and magnitude of mood swings (‘’mood stabilizer’’)àusually an antidepressant/antipsychotic is also required MOA: (follow figure above) - Prevent recycling of inositolàdecreased IP3 + DAG (diacylglycerol)àinterfere with actions of Gq/s-coupled receptorsà↓ second messengersà↓neuronal activity in pathologically overactive circuitsàmood stabilization

Answer 119

Antiepileptics used in partial seizures and generalized tonic-clonic seizures MOA: - Inhibition of VG Na+-channel Effect: - Prevent seizure propagation, but not initiation

Answer 120

Antiepileptics used in partial seizures and generalized tonic-clonic seizure MOA: - Inhibition of VG Na+-channel Effect: - Prevent seizure propagation, but not initiation

Answer 121

Antiepileptics used in partial seizures and generalized tonic-clonic seizures MOA: - Inhibits GABA metabolism - May also block Na+ / Ca2+ channels at higher concentrations Effect: - Prevent tonic-clonic or partial seizures (2nd or 3rd in line due to SE)

Answer 122

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs. MOA: - Inhibits T-type Ca2+ channels in the thalamus - Narrow spectrum Indication: - Absence seizures ONLY!

Answer 123

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs MOA + Effect: - Inhibits VG Na+ channels, T-type Ca2+ channels - Enhances GABA transmission, decreases glutamate Indication: - All seizures (including absence seizures)àbroad spectrum - Bipolar disorders, migraine

Answer 124

Antiepileptics used in absence seizures. “The Broad spectrum” antiepileptic drugs MOA: - Inhibits Na+ channels + reduces glutamate release Indication: - Most seizuresàbroad spectrum - Not teratogenic (unlike others)àcan be given to pregnant women

Answer 125

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs. MOA + Effect: - Benzodiazepine - Enhances effect of GABA Indication: - Absence seizure (first line), panic + anxiety disordersl

Answer 126

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs. MOA + Effect: - Prevents synaptic release of glutamate (SV2A receptor blockade) Indication: - Tonic-clonic, partial, myoclonic seizures in childrenàbroad spectrum - Not teratogenicàcan be given to pregnant women

Answer 127

Antiepileptics used in partial seizures and generalized tonic-clonic seizures except for the “broad spectrum MOA: - Inhibits GABA metabolism (GABA-transaminase inhibitor) Effect: - Decreased GABA metabolismàmore GABA released Indication: - Partial seizures + infantile (juvenile) spasm

Answer 128

Drugs used in Parkinson’s disease MOA: - Levodopa is the metabolic precursor of dopamine Effect: - Levodopa can cross the BBB (dopamine cannot) and increase the synthesis of dopamine in the brain - Levodopa is converted by DOPA-decarboxylase à only 1-3% enters brain due to extensive peripheral metabolism by the enzymeàgive carbidopa, which is a peripheral inhibitor of the enzyme

Answer 129

Drugs acting in the extrapyramidal motoric system. Drugs used in Parkinson’s disease MOA: - Dopamine D2 agonists (non-ergot derivatives) Effect: - Longer duration of action than levodopa and effective in patients with fluctuations in response to levodopa - Pramipexole is a potential anti-oxidant

Answer 130

Drugs acting on extrapiramidal system Drugs against Parkinson’s Disease MOA: - Selective + reversible MAO-B inhibitor Effect: - Decreases metabolism of dopamine à increased dopamine activity in the brain - No ‘’cheese effect’’ as seen with non-selective MAO inhibitors - Neuroprotective (enhancement of scavenger function)

Answer 131

Drugs acting on extrapyramidal system Drugs agains Parkinson’s disease MOA: - Antiviral drug (influenza prevention) Effect: - Uncertain mechanism à increased dopamine release / block dopamine reuptake, block muscarinic receptors - Weaker than levodopa and tolerance develops against it

Answer 132

Drugs acting on extrapyramidal system Drugs against Parkinson disease MOA: - Muscarinic receptor antagonist Effect: - Decreases resting tremor and rigidity, but little effect against bradykinesia

Answer 133

Drugs acting on extrapyramidal system Drugs acting against Alzheimer’s Disease MOA: - Glutamate NMDA receptor blocker Effect + Indication: - Stimulation of CNS glutamate receptors appears to be critical in formation of certain memories, but overstimulation may result in excitotoxicity Side-effects: - Confusion, agitation

Answer 134

Drug acting on extrapyramidal system Drugs used for Alzheimer’s disease MOA: - ACh-esterase inhibitor (centrally-acting) Effect + Indication: - 1st line agent for Alzheimer’s diseaseàprovide moderate reduction in rate of loss of cognitive function

Answer 135

Drug caring on extrapyramidal system Drug used for Alzheimer’s disease Interferes with NT release by binding to synaptic vesicle protein (SV2A) - Used as cognition enhancers and in treatment of ADHD (attention deficit hyperactivity disorder), Parkinson’s disease and schizophrenia