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Pharmacology Year 2 > All Drugs > Flashcards

All Drugs Flashcards

1
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Reserpine?

A

a) Antipsychotic

b) Storage vesicles for monoamine neurotransmitter

c) Depletes monoamines (e.g. dopamine) stored in vesicles

d) Antipsychotic as decreases positive symptoms of schizophrenia but causes depression side effects due to decreasing dopamine transmission

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2
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Iproniazid?

A

a) MAOI (monoamine oxidase inhibitor)

b) Monoamine oxidase enzyme type a

c) MAO inhibitor increasing monoamine neurotransmitter conc as less are metabolised.

d) Anti-depressant as increases dopamine transmission but cause NA depletion in sympathetic terminals causes postural hypotension

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3
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Phenylzine (Phenelzine)?

A

a) MAOI (monoamine oxidase inhibitor)

b) Monoamine oxidase enzyme type a

c) MAO inhibitor increasing monoamine neurotransmitter conc as less are metabolised.
>Is an irreversible non-competitive inhibitor so has long lasting effects.

d) Anti-depressant as increases dopamine transmission but cause NA depletion in sympathetic terminals causes postural hypotension

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4
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Moclobemide?

A

a) MAOI (monoamine oxidase inhibitor)

b) Monoamine oxidase enzyme type a

c) Very selectively blocks MAO enzymes.

d) Anti-depressant as increased dopamine transmission, and due to selectivity avoids Side effects such as hypotension (due to NA depletion).

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5
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Imipramine?

A

a) Classical Tricyclic anti-depressant

b) Re-uptake transporters for all monoamine neurotransmitters on pre-synaptic membrane

c) blocks re-uptake so neurotransmitter remains in synapse for longer

d) Anti-depressant as increases dopamine transmission.

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6
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of fluoxetine/prozac?

A

a) Selective serotonin re-uptake inhibitor (SSRi)

b) Re-uptake transporter for 5-HT (serotonin)

c) Blocks re-uptake of serotonin so it stays in the cleft for longer.

d) Anti-depressant as increases 5-HT transmission.

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7
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of citalopram?

A

a) Selective serotonin re-uptake inhibitor (SSRi)

b) Re-uptake transporter for 5-HT (serotonin)

c) Blocks re-uptake of serotonin so it stays in the cleft for longer.

d) Anti-depressant as increases 5-HT transmission.

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8
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of reboxetine?

A

a) Selective noradrenaline re-uptake transporter inhibitor

b) Re-uptake transporter for NA

c) Blocks reuptake of NA

d) Anti-depressant as increases NA signalling, leads to hypertension (high blood pressure) due to more NA transmission.

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9
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Side effect of LSD?

A

a) Serotonin receptor agonist

b) 5 HT2A receptor

c) activates 5 HT2A serotonin receptor.

d) Is a psychedelic causing positive symptoms of schizophrenia.

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10
Q

What is the c) Mechanism of Action d) Clinical use of Lithium?

A

c) Enter neurons through hyperactive Na channels, reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission

d) Anti-depressant for bipolar depression.

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11
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Amphetamines?

A

a) Central nervous system stimulant

b) Storage vesicles of monoamine neurotransmitters

c) Act as a false neurotransmitter, taken up into storage vesicles, amine neurotransmitters pushed into cytosol until conc gradient favors exit of amines out of cell instead of re-uptake, increasing NA and DA signalling.
>Independent of AP firing.

d) Treat ADHD and narcolepsy (can’t control sleep)

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12
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Cocaine?

A

a) CNS stimulant

b) monoamine neurotramitter re-uptake transporters

c) Inhibits re-uptake transporters so monoamines stay in cleft for longer.

d) Leads to increased motor activity in SNS and PNS

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13
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Ketamine?

A

a) Dissociative anaesthetic

b) NMDA (Glutamate receptor)

c) Inhibits NMDA receptor activation causing less CNS APs firing.

d) Anaesthetic as causes analgesia but doesn’t cause full loss of consciousness (disadvantage)
>Sub anaesthetic doses are good anti-depressants
>Gives rise to positive schizophrenic symptoms

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14
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of Phencyclidine (PCP)?

A

a) Dissociative anaesthetic (similar to ketamine)

b) NMDA (Glutamate receptor)

c) Inhibits NMDA receptor activation causing less CNS APs firing.

d) Anaesthetic as causes analgesia but doesn’t cause full loss of consciousness (disadvantage)
>Sub anaesthetic doses are good anti-depressants
>Gives rise to positive schizophrenic symptoms

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15
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of chlorpromazine?

A

a) First generation antipsychotics (neuroleptics)

b) D2 receptors

c) antagonists of D2 receptors decreasing dopamine transmission

d) Antipsychotic, treats schizophrenia but causes Parkinson’s like symptoms and prolactin secretion

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16
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of haloperidol?

A

a) First generation antipsychotics (neuroleptics/ typical)

b) D2 receptors

c) antagonists of D2 receptors decreasing dopamine transmission

d) Antipsychotic, treats schizophrenia but causes Parkinson’s like symptoms and prolactin secretion

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17
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of clozapine?

A

a) Second generation antipsychotics (atypical)

b) D2 receptor

c) Antagonists of D2 receptors decreasing dopamine transmission in mesocortical pathway not in Nigral striatal (motor control) and neurohypophysial (endocrine control) pathways.

d) antipsychotic to treat schizophrenia without Parkinson’s and lactation side effects

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18
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of rispiridone?

A

a) Second generation antipsychotics (atypical)

b) D2 receptor

c) Antagonists of D2 receptors decreasing dopamine transmission in mesocortical pathway not in Nigral striatal (motor control) and neurohypophysial (endocrine control) pathways.

d) antipsychotic to treat schizophrenia without Parkinson’s and lactation side effects

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19
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of PTZ?

A

a) CNS stimulating

b) GABAA receptors

c) Blocks GABAA receptors decreasing inhibitory regulation of CNS causing seizures

d) Induces seizures for chemical models of epilepsy.

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20
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of clonazepam?

A

a) Benzodiazepine

b) GABAA receptor

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.
>Increases the frequency the channel opens

d) Anti-epileptic drug

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21
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of diazepam?

A

a) Benzodiazepine

b) GABAA receptor

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.
>Increases the frequency the channel opens

d) Anti-epileptic drug and anxiolytic (anti-anxiety)

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22
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of phenobarbitone?

A

a) Barbiturate

b) GABAA receptor

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.
>Increases duration when channel opens

d) Antiepileptic

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23
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of vigabatrin?

A

a) GABA Metabolic inhibitor

b) GABA Transaminase enzyme

c) suicide inhibitor blocking GABA Transaminase, decreasing the metabolism of GABA menacing more CNS inhibitory regulation

d) Anti-Epileptic Drugs (anti-convulsant)

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24
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of valproate?

A

a) GABA Metabolic inhibitor

b) GABA Transaminase enzyme

c) suicide inhibitor blocking GABA Transaminase, decreasing the metabolism of GABA menacing more CNS inhibitory regulation

d) Anti-Epileptic Drugs (anti-convulsant)

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25
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of phenytoin?

A

a) Use-dependant sodium channel inhibitors

b) voltage gated NA channels

c) Binding to the NA channels prolongs the duration of the inactive state (keeps the inactivating particle blocking)

d) Antiepileptic

26
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of carbamazepine?

A

aa) Use-dependant sodium channel inhibitors

b) voltage gated NA channels

c) Binding to the NA channels prolongs the duration of the inactive state (keeps the inactivating particle blocking)

d) Antiepileptic

27
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of ethosuximide?

A

a) 3-Ca2+ channel blocker

b) 3-Ca2+ channels

c) Blocks T-type Ca channels mediating AP firing in oscillatory behaviour that cause absence seizures

d) Antiepileptic

28
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of pregabalin?

A

a) 4-Ca2+ channel trafficking inhibitor

b) α2δ subunit of Ca2+ channels

c) Bind to α2δ subunit of Ca2+ channels to reduce trafficking of channel to plasma membrane, decreasing AP firing causing seizures.

d) Antiepileptic and antidepressant

29
Q

What is the b) Target c) Mechanism of Action d) Clinical use of levetiracetam?

A

b) Binds to proteins on synaptic vesicles.

c) Decreases the amount of glutamate released from synaptic vesicles, decreasing the excitatory effect in CNS.

d) Antiepileptic (anti-convulsant)

30
Q

What is the clinical use of cannabidiol?

A

It is the non-psychoactive component of cannabis and can act as a anti-epileptic (anti-convulsant)

31
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical of muscimol?

A

a) Orthosteric agonist for GABAA receptors

b) GABAA receptors

c) Binds to orthosteric site of GABAA causing inhibitory regulation on CNS

d) Anxiolytic

32
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Side effects of bicuculline?

A

a) Orthosteric competitive antagonist for GABAA receptors

b) GABAA receptors

c) Binds to orthosteric site of GABAA, decreases the response caused by GABA, reducing inhibitory regulation so overexcitation of CNS is caused.

d) Causes anxiety and seizures due to lack of inhibitory regulation of the CNS

33
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Side effects use of picrotoxin?

A

a) Orthosteric non-competitive antagonist for GABAA receptors

b) GABAA receptors

c) Binds to orthosteric site of GABAA, decreases the response caused by GABA, reducing inhibitory regulation so overexcitation of CNS is caused.

d) Causes anxiety and seizures due to lack of inhibitory regulation of the CNS

34
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of flumazenil?

A

a) Allosteric competitive antagonist for GABAA receptors

b) GABAA receptors

c) Reduces the effect of agonists bound to GABAA receptors, so decreases the inhibitory regulation of the CNS

d) Reduce effects of an overdose of an agonist.

35
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Side effects of flunitrazepam/rohypnol?

A

a) Benzodiazepine

b) GABAA receptors

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.

d) Causes anterograde amnesia (prevents memory of events experienced while under their influence).

36
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of zolpidem?

A

a) Short acting Benzodiazepine

b) GABAA receptor

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.
>Increases the frequency the channel opens

d) Anxiolytic

37
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of propranolol?

A

a) Beta-blocker

b) B1 adrenergic receptor

c) Inhibits NA from binding to B1 adrenergic receptors decreasing increase in heart rate lowering blood pressure.

d) Anxiolytic

38
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of buspirone?

A

a) 5-HT1A receptor partial agonist

b) 5-HT1A receptor

c) Bind to 5-HT1a receptors decreasing heart rate and blood pressure.

d) Anxiolytic for generalised anxiety (not phobias)

39
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of olanzepine?

A

a) Atypical (second-generation) antipsychotic

b) D2 receptors

c) Blocks D2 receptors in mesolimbic pathway decreasing dopamine transmission.

d) Anxiolytic for generalised anxiety and PTSD

40
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of lorazepam?

A

a) Short acting Benzodiazepine

b) GABAA receptor

c) Positive allosteric modulator for GABAA receptor, so when GABA binds it increases the inhibitory effect.
>Increases the frequency the channel opens

d) Anxiolytic and hypnotic (treats insomnia associated with anxiety)

41
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of promethazine?

A

a) Anti-histamines

b) H1 receptors

c) H1 receptor antagonist

d) Hypnotic (treats insomnia associated with anxiety)

42
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of chloroform?

A

a) Volatile anaesthetic

b) GABAA receptor alpha and beta subunits and Two Pore Domain K channels (regulate resting mV of neurons)

c) Activate GABAA causing inhibitory regulation of CNS and activation of K+ channels hyperpolarises neuron resting mV so less APs fire.

d) General anaesthetic

43
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of nitrous oxide?

A

a) Inhaled General anaesthetic

b) GABAA receptor

c) Increases effect of GABAA receptor, increases inhibitory regulation of CNS

d) General anaesthetic only causing analgesia (still conscious)

44
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical e) side effects use of isoflurane?

A

a) Halogenated general anaesthetic

b) GABAA receptor

c) Increases effect of GABAA receptor, increases inhibitory regulation of CNS

d) General anaesthetic

e) Malignant hypothermia is triggered when people have a mutation with their ryanodine receptors.

45
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of thiopental?

A

a) Barbiturate

b) GABAA receptor

c) positive allosteric modulator increasing inhibitory effects of GABAA receptor

d) General anaesthetic

46
Q

What is the a) Drug class b) Clinical use c) an advantage of of etomidate?

A

a) Intravenous anaesthetic

b) General anaesthetic

c) Doesn’t cause cardiovascular depression like other intravenous anaesthetics do

47
Q

What is the a) Drug class b) Clinical use c) an advantage of of Propofol?

A

a) Intravenous anaesthetic

b) General anaesthetic

c) is metabolised quickly, so is easy to change conc for general anaesthetics non toxic levels and won’t leave a hangover.

48
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of dantrolene?

A

a) Inhibitor of ryanodine receptors

b) Ryanodine receptors

c) Inhibits ryanodine receptors from causing muscle contraction.

d) Counteracts malignant hyperthermia

49
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of morphine?

A

a) Opioid

b) Mu-opioid receptors

c) Activate mu-opioid receptors (agonist)

d) Analgesic

50
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of heroin?

A

a) Synthetic opioid (stronger than morphine)

b) Mu-opioid receptors

c) Activate mu-opioid receptors (agonist)

d) Analgesic

51
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of aspirin?

A

a) Non-Steroidal Anti-inflammatory Drugs/ Suicide inhibitor for COX1 (Cyclooxygenase 1) enzyme

b) COX1 enzyme

c) Inhibits COX1 as a suicide inhibitor decreasing prostaglandins and thromboxane’s which decreases the inflammatory response

d) Anti-inflammatory and antithrombotic

52
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of ibuprofen?

A

a) Non-Steroidal Anti-inflammatory Drugs/ COX 2 selective inhibitor

b) COX 2

c) Inhibits COX2 as a suicide inhibitor decreasing prostaglandins and thromboxane’s which decreases the inflammatory response

d) Anti-inflammatory

53
Q

What is the a) Drug class b) Target c) Side effects of rofecoxib?

A

a) COX2 selective drug

b) COX2 enzyme

c) cardiovascular disease due to increase of NA causing increased blood pressure.

54
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of paracetamol?

A

a) Non-Steroidal Anti-inflammatory Drugs/ COX 2 selective inhibitor

b) COX 1 and 3

c) Inhibits COX1 as a competitive inhibitor decreasing prostaglandins and thromboxane’s which decreases the inflammatory response

d) Anti-inflammatory, Analgesia and Antipyretic (lowers temp)

55
Q

What is the Clinical use of misoprostol?

A

Acts as a prostaglandin to reduce loss of gut mucus so reduces gut ulcers caused by NSAIDs like Aspirin

56
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of methotrexate?

A

a) Methotrexate

b) Folic acid

c) Antagonist for folic acid causing cytotoxic (toxic to cells preventing cell growth) and immunosuppressant activity

d) High concentrations of this are useful for cancer treatment with bad Side effects, but low conc treats arthritis (anti-inflammatory) with low side effects

57
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of sulfasalazine?

A

a) Sulfa drug

b) Not cleary Known

c) Not clearly known

d) anti-inflammatory for chronic inflammatory bowel disease

58
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of cyclosporin?

A

a) Steroid drug

b) Calcineurin enzyme

c) Inhibits induction stage of inflammatory response by binding to Calcineurin (phosphatase enzyme)
so it can no longer activate transcription factor NFΚB (K=Kappa), NFΚB can no longer drive increase the in production and secretion of cytokines including IL-2 and IL-1 that drive the inflammatory response.

d) Anti-inflammatory

59
Q

What is the a) Drug class b) Clinical use of adalimumab?

A

a) Monoclonal antibody (has mab in name)

b) Anti-inflammatory to treat rheumatoid arthritis.

60
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of salbutamol?

A

a) Bronchodilator

b) B2 adrenoreceptors in airway smooth muscle

c) Antagonist for B2 adrenoreceptors causing relaxation of smooth muscle so airways dilate (open up).

d) anti-asthmatic (anti-inflammatory)

61
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of prednisolone?

A

a) Glucocorticoids (steroid drug)

b) Nuclear receptors on DNA

c) Inhibits transcription of genes that make cytokines which decreases the immune inflammatory response

d) anti-inflammatory

62
Q

What is the a) Drug class b) Target c) Mechanism of Action d) Clinical use of omalizumab?

A

a) Monoclonal antibody (mab in name)

b) IgE antibody

c) binds to IgE, antibody preventing it from binding to receptors so an inflammatory response doesn’t occur.

d) Anti-inflammatory agent

Pharmacology Year 2 (8 decks)

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