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Drugs List > Block 3 Drugs > Flashcards

Block 3 Drugs Flashcards

1
Q

Selective Serotonin Reuptake Inhbitors (SSRIs)

Drugs

MoA

Side Effects

A

Antidepressants

  • Citalopram
  • Sertraline

Increases 5-HT levels by inhibiting reuptake pump.

Side Effects:

  • Slow onset, can increase depressive symptoms initially
  • Nausea
  • Sleep disorders
  • Sexual dysfunction
  • Increased bleeding
  • Serotonin syndrome (increased 5-HT levels)- Emergency
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2
Q

Atypical Antidepressants: Noradrenaline reuptake inhibitors

A
  • Raboxetine

​Inhibits the reuptake pump for noradrenaline

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3
Q

Atypical Antidepressants: Serotonin Noradrenaline Reuptake Inhibitors

A
  • Venlafaxine

Inhibits the reuptake pumps of both 5-HT and noradrenaline

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4
Q

Atypical Antidepressants: 5HT partial agonists

MoA

A
  • Buspirone

Slows flow of neuronal impulses to allow time for build up of 5HT in presynaptic vesicles.

Decreases number of receptors, so that the next time an action potential fires, it is much more effective.

Fewer side effects than SSRIs

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5
Q

Atypical antidepressants: Melatonin Agonist

MoA

A
  • Agomelatine

Increases slow wave sleep to prolong sleep duration and reset sleep patterns.

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6
Q

Tricyclic Antidepressants

A
  • Amitriptyline
  • Nortriptyline

5 Main actions:

  • Therapeutic effects:
    • 5HT reuptake inhibitor
    • Noradrenaline reuptake inhibitor
  • Side effect causing:
    • A1 adrenoceptor antagonist
      • Postural hypotension
    • H1 receptor antagonist:
      • Sedation
    • M1 receptor antagonist
      • Cardiac dysrhythmia

Other side effects:​

  • Confusion
  • Mania
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7
Q

Antidepressants: Monoamine Oxidase Inhibitors A form

MoA

Side effects

A

Antidepressants

  • Moclobemide

Increases 5-HT and noradrenaline levels by reversibly inhibiting enzymatic breakdown.

Side effects:

  • Also affects dopamine levels
  • DO NOT USE WITH TCAs/SSRIs
  • Interacts with cheese (contains tyramine)
  • Postural hypotension
  • Restlessness
  • Convulsions
  • Sleep disorders
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8
Q

Atypical antidepressants: a2-adrenoceptor antagonist

MoA

Side Effects

A
  • Mirtazipine

Increase neurotransmitter release by inhibiting a2 receptors which normally slow transmitter release.

Side Effects:

  • Decreased vascular flow in extremities
  • Postural hypotension
  • Fatigue
  • Bronchoconstriction
  • Cardiac failure
  • Bradycardia
  • Sleep disorders
  • Impotence
  • Depression
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9
Q

Which neurotransmitter is responsible for altered arousal in TCAs?

A

Histaminergic

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10
Q

Which common antidepressant can be used to treat neuropathic pain?

A

Nortriptyline

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11
Q

Anti-epileptics drugs: Sodium Channel Blockers

Uses

MoA

Side Effects

A
  • Sodium valproate
  • Lamotrigine
  • Carbamazepine

Blocks voltage gated Na+ channel in inactivated state

Side Effects:

  • Sodium Valproate: Teratogenicity: foetal developmental defects
  • Cognitive impairment
  • Visual impairment
  • Peripheral neuropathy
  • Gum hyperplasia
  • Anaemia
  • Osteomalacia
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12
Q

What pharmacological treatments are used for focal and focal to generalised seizures?

A

First line:

  • Carbamazepine
  • Lamotrigine

Also:

  • Sodium valproate
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13
Q

What pharmacological treatments are used for generalised tonic-clonic seizures?

A

First line:

  • Sodium valproate
  • Lamotrigine

Also:

  • Carbamazepine
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14
Q

What drugs are used for typical generalised absence seizures?

A

First line:

  • Ethosuximide
  • Sodium valproate

Also:

  • Lamotrigine
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15
Q

What drugs are used for treatment of status epilepticus generalised tonic-clonic?

A
  • Commence IV Lorazepam (repeated after 10 mins)/buccal midazolam/IV diazepam
  • Buccal midazolam/rectal diazepam if no resus facilities available
  • After 25 mins: IV phenobarbital sodium
  • After 45 mins: Anaesthetise (propofol)
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16
Q

How is non-epileptic attack disorder treated?

A
  • Cognitive behavioural therapy/psychotherapy
  • Antidepressants/antipsychotics
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17
Q

What drugs are used in a generalised myoclonic seizure?

A

First line:

  • Sodium valproate
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18
Q

What drugs are used for generalised absence atypical/ generalised atonic/ generalised tonic seizures?

A

First line:

  • Sodium valproate

Second line (adjunct)

  • Lamotrigine
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19
Q

What is a major side effect of anti-epileptic drugs?

What are the symptoms?

How is it treated?

A

Antiepileptic Hypersensitivity Syndrome

  • 1-8 weeks after initiation of treatment
  • Initial signs: rash, ever, swollen lymph nodes
  • Severe signs: blood, liver, kidney and respiratory abnormalities, vasculitis and organ failure.

Treatment:

  • Withdrawal of drug immediately (possibility of rebound seizure)
  • Topical steroids and antihistamines for rash
  • Systemic corticosteroids can be used
    *
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20
Q

Benzodiazepines

Drugs

Uses

MoA

Side Effects

A
  • Midazolam (fast recovery time)
  • Lorazepam
  • Diazepam (mild)
  • Temazepam (short acting)

Epilepsy (status epilepticus)

Co-agonist (positive allosteric modulators) which bind to the y-subunit of the GABAA receptor to increase action of GABA. Reduces neuronal transmission by increasing chloride entry into the cell leading to hyperpolarisation and decreased likelihood of action potential firing.

Uses:

  • Epilepsy
  • Anxiety
  • Imsomnia
  • Sedation

Side Effects:

  • Withdrawal on termination
  • Tolerance and dependency
  • Impaired motor coordination
  • Sedation
  • Impaired cognitive function
  • Retrograde amnesia
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21
Q

Anti-epileptic drugs: Calcium channel blockers

Drugs

MoA

A
  • Ethosuximide

T-type Ca2+ channel blocker

  • Gabapentin

Calcium channel blocker

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22
Q

Barbiturates

Drugs

Uses

MoA

Side Effects

A
  • Phenobarbital
  • Pentobarbital
  • Primidone

Used as anaesthetics/anxiolytics

Co-agonist of the GABAA receptor (B subunit) to increase activity.

Reduces neuronal transmission by enhancing inhibition

Side Effects:

  • Withdrawal on termination
  • Tolerance and dependency
  • Impaired motor coordination
  • Sedation
  • Impaired cognitive function
  • Retrograde amnesia
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23
Q

NSAIDs: Non selective COX inhibitors

Drugs

MoA

Side effects

A
  • Ibuprofen
  • Diclofenac
  • Aspirin
  • Naproxen

Block production of prostaglandins by inhibiting cyclo-oxygenase enzyme:

  • COX1 : normal cell function
  • COX2 : inflammation
  • COX3 : fuck knows

Inhibiting COX2 reduces production of inflammatory prostaglandins therefore reduce activation of prostanoid receptor and Na+ channel activation.

Reduced Na+ channel activation leads to decreased depolarisation and less pain transmission.

Side Effects:

Inhibiting COX1 inhibits production of PGE1 and PGI2 which have a role in normal physiological processes in platelets, endothelium, kidney, stomach and intestinal function.

  • Bleeding
  • Stomach ulcers
  • Heartburn
  • Nausea/ vomiting
  • Diarrhoea
  • Headache
  • Tinnitus
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24
Q

Paracetamol

MoA

Uses

A

Weak analgesic/ anti-pyretic

Non-selective inhibitor of COX enzymes

Used for mild nociceptive pain

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25
Q

NSAIDs: Selective COX2 inhibitors

Drugs

MoA

Uses

A
  • Celecoxib
  • Etoricoxib

Selective inhibition of COX2 enzyme inhibiting inflammation.

Less GI side effects

26
Q

Weak Opioids

Drugs

MoA

Uses

Side effects

A
  • Codeine
  • Dihydrocodeine

Mimic endogenous opioids acting on opioid receptors µ, K, delta and ORL-1. Decrease neuronal transmission by:

  • Hyperpolarising the cell so it is less likely to fire AP when simulus arrives:
    • Decreases opening of voltage gated Na+ channels
    • Increases K+ outflow via KATP and KIR channels
  • Reduces exocytosis of transmitters
  • Decreases Ca2+ release from intracellular stores

Uses:

  • Chronic and acute pain

Side effects:

  • Constipation (reduced GI motility)
  • Respiratory depression
  • Tolerance and dependance, withdrawal
  • Miosis
27
Q

What are the symptoms of NSAID intoxication?

A

Tinnitus, ototoxicity, deafness

Aspiration pneumonitis, pulmonary oedema, alkalosis

Tachycardia, HTN, dysrhythmias

Depression, seizures, encephalopathy, delirium

Pancreatitis

Renal failure

Coma

28
Q

Strong Opioids

Drugs

MoA

Uses

Side effects

A
  • Morphine
  • Diamorphine

Mimic endogenous opioids acting on opioid receptors µ, K, delta and ORL-1. Decrease neuronal transmission by:

  • Hyperpolarises the cell so it is less likely to fire when AP arrives:
    • Decreases opening of voltage gated Ca2+ channels
    • Increases K+ outflow via KATP and KIR channels
  • Reduces exocytosis of transmitter vesicles
  • Decreases Ca2+ release from intracellular stores

(Hyperpolarises cell so it is less likely to fire when simulus arrives)

Uses:

  • Coronary care
  • Cancer care
  • Palliative care

Side effects:

  • Respiratory depression
  • Constipation (reduced GI motility)
  • Sedation
  • Tolerance and dependance, withdrawal
  • Miosis
29
Q

Partial/mixed opioid agonists/antagonists

Drugs

MoA

Uses

Side effects

A
  • Buprenorphine

Agonist of µ opioid receptors and antagonist of K opioid receptors.

Uses:

  • Analgesia
  • Opioid addiction
30
Q

Opioid receptor antagonists

Drugs

MoA

Uses

A
  • Naloxone (short half life)
  • Naltrexone (longer half life)

Competitive antagonist of opioid receptors reducing the effect of opioids.

Uses:

  • Opioid overdose
31
Q

What are the areas of opioid action?

A

Periaqueductal grey

Nucleus raphe paragigantocellularis

Dorsal Horn

Periphery

32
Q

Drugs used for opioid addiction

Drugs

MoA

A
  • Buprenorphine
  • Methadone

Buprenorphine: µ agonist and K antagonist

Methadone: µ agonist

33
Q

Which drugs are used to treat neuropathic pain?

A

Tricyclic anti-depressants

Gabapentin

Pregabalin

Carbamazepine

34
Q

Synthetic dopamine agonists

Drugs

MoA

Uses

Side effects

A
  • Pramipexole
  • Ropinirole
  • Rotigotine

Synthetic dopamine, act on dopamine receptors (primarily D2) to replace lost dopamine

Less overall improvement than levodopa, more psychiatric side effects.

Uses:

  • Younger PD patients to delay treatment with levodopa
  • First line for initial treatment
  • Can be used in conjunction with levodopa at later stages

Side Effects:

  • Psychiatric symptoms (due to action on mesocortical and mesolimbic pathways)
  • Nausea and vomiting
  • Sudden onset sleep/ drowsiness
  • On-off effects
  • Hypotension
  • Tachycardia
35
Q

Describe the on-off effects of dopamine based treatments for Parkinson’s disease

What can be used to ‘bridge the gap’ between dopamine treatments?

A

In the later stages of Parkinson’s disease, there can be rapid wear on and wear off of the effects of dopamine treatments.

Wear off between doses causes relapse of symptoms.

Drugs used between doses:

  • Apomorphine
  • Domperidone (always administered prophylactically before apomorphine dose)
  • Duodopa (gel form of L-dopa inserted into stomach)
36
Q

Levodopa

Uses

MoA

Side effects

A

Dopamine precursor: crosses blood brain barrier and is metabolised into dopamine to replace that lost. Works on dopamine receptors to restore activity in the nigrostriatal pathway.

Uses:

  • Parkinson’s disease (as late as possible)

Side effects:

  • Psychiatric symptoms (due to action on mesocortical and mesolimbic pathways)
  • Nausea and vomiting
  • Sudden onset sleep/ drowsiness
  • On-off effects
  • Hypotension
  • Tachycardia
37
Q

Anticholinergics

Drugs

MoA

Uses

Side Effects

A
  • Orphenadrine
  • Procyclidine
  • Trihexphenidyl

Inhibits cholinergic fibres from the striatum to the globus pallidus that moderate GABAergic cells and prevents them from inhibiting the direct pathway and increase effects of the indirect pathway.

Uses:

  • Iatrogenic parkinsonism (drug-induced)
  • Poor effects on idiopathic parkinsonism

Side effects:

  • Can reduce absorption of levodopa
38
Q

Dopa-decarboxylase inhibitors

Drugs

MoA

Uses

A
  • Carbidopa
  • Benserazide

Prevents the breakdown of levodopa in the periphery by dopa-decarboxylase enzyme allowing more to cross the blood brain barrier and be converted into dopamine.

Uses:

  • In combination with levodopa in Parkinsonism
39
Q

COM-T Inhibitors

Drugs

MoA

Uses

A
  • Entecapone
  • Tolcapone

Prevents breakdown of levodopa in the CNS by Catechol-O-methyltransferase (COM-T) so more is available to be converted to dopamine.

Uses:

  • Alongside levodopa for Parkinsonism
40
Q

MAOI-B Inhibitors

(monoamineoxidase- B form inhbitors)

Drugs

MoA

Uses

A
  • Rasagiline
  • Selegiline

Prevent the breakdown of levodopa in the CNS by monoamineoxidase-B meaning more is available to be converted into dopamine.

Uses:

  • Alongside levodopa in Parkinsonism
41
Q

Dopamine-depleting drugs

Drugs

MoA

Uses

Side effects

A
  • Tetrabenazine

Inhibits VMAT2 (vesicular monoamine transporter) within basal ganglia, preventing transport of dopamine into presynaptic vesicles therefore less released into the synaptic cleft.

Uses:

  • Huntington’s disease

Side effects:

  • Affects all monoamines: 5-HT and NA
    • Can cause depression
42
Q

First generation antipsychotics

Drugs

MoA

Uses

Side effects

A
  • Haloperidol
  • Chlorpromazine

Selective dopamine D2 receptor antagonists. Also affect M1, H1, alpha1 receptors.

Low efficacy (30% non-responders)

Uses:

  • Schizophrenia
  • Haloperidol: short term management of extreme or aggressive behaviour, rapid tranquilisation
  • Huntington’s: haloperidol

Side effects:

  • Extrapyramidal symptoms (result of altering activity of nigrostriatal pathways):
    • Dystonias
    • Akathisia
    • Parkinsonism
    • Sedation
    • Seizures
    • Hypotension
    • Hypothermia
    • Hypersensitivity
  • Chlorpromazine: agranulocytosis
  • Tardive dyskinesia from prolonged use (choreiform movements, grimacing, tongue protruding)
43
Q

What is thought to cause tardive dyskinesia in prolonged use of first generation anti-psychotics?

A

Oxidative neurodegeneration caused by increased glutamatergic transmission which results from the down-regulation of the dopamine system.

44
Q

Second generation anti-psychotics

Drugs

MoA

Uses

Side effects

A
  • ​Amisulpride: first line treatment
    • ​5HT7 and Dopamine (D1 & D2) antagonist (mesolimbic pathway)
  • Risperidone
    • ​5HT2A and Dopamine antagonist
  • Clozapine: gold standard but many side effects
    • ​5HT2A and domapine antagonist

Also affect H1, M1 and a1 receptors + interact with reuptake mechanisms.

Uses:

  • Schizophrenia: risperidone more effective at treating negative symptoms
  • Huntington’s: risperidone
  • Chorea

Side effects:

  • Less extrapyramidal symptoms than first generation due to higher affinity for mesolimbic and mesocortical pathways than nigrostriatal.
  • More cholinergic side effects than first gen:
45
Q

Local anaesthetics

Drugs

MoA

Side effects

A
  • Lidocaine
  • Bupivicaine
  • Levobupivicaine

Block voltage gated sodium channels. 2 ways:

  • Directly entering open sodium channels (use-dependence, more channels open = bigger the effect)
  • Accessing sodium channels by crossing axonal membrane and binding from the inside

Uses:

  • Lidocaine: regional IV anaesthesia, nerve block, dental and topical.
  • Bupivicane and Levobupivicane: local infiltration, regional IV anaesthesia, epidural, peripheral nerve block, sympathetic block.
    • Levobupivicane less cardiotoxic effects.

Side Effects:

  • Local irritation and inflammation
    • Exacerbated by local vasoconstrictors →ischamia
  • Systemic effects and anaphylaxis rare.
46
Q

General IV Anaesthetics

Drugs

MoA

Side effects

A
  • Propofol
  • Ketamine
  • Midazolam

Suppress action of the CNS by acting on:

  • Inhibitory pathways (midazolam- increases activity at the GABA receptor, positive allosteric modulator )
  • Excitatory pathways (ketamine- NMDA glutamatergic receptor antagonist, prevents movement of sodium and calcium into the cell)
  • Profol- unclear

Uses:

  • Used to initiate anaesthesia- not generally used for maintenance (propofol is the exception) due to accumulation effects and slow redistribution.

Side effects:

  • Decreased cardiac contractility
  • Respiratory depression (in overdose leading to respiratory failure and death)
  • Decreased CNS function
  • Reduced sympathetic activity
47
Q

Anaesthetics: IV opioids

Drugs

MoA

Uses

Side effects

A
  • Fentanyl
  • Alfentanil
  • Remifentanil

Opioid receptor agonists.

Uses:

  • Given at induction to aid analgesia and to reduce the amount of anaesthetic required through sedative effect.
  • Counteract the effects of invasive treatments: raised BP, HR and RR caused by stress.

Side effects:

  • Respiratory depression (care must be taken when given alongside other opioids)
48
Q

Epidural drugs

A
  • Bupivicaine
  • Lidocaine
49
Q

Depolarising neuromuscular blockers

Drugs

MoA

Uses

Side effects

A
  • Neostigmine
    • ​Non-competitive block of acetylcholinesterase (AchE) breakdown of Ach to increase levels of Ach in the junctional cleft. Causes muscle paralysis by overloading the system, activating all Ach receptors at maximum and leaving no room for additional movement; similar to depolarising NMBs.
  • ​Suxamethonium
    • ​IV only
    • Rapid action, muscle relaxation within 1 minute: needs continuous infusion.
    • Non-competitive agonists of ACh receptors causing prolonged depolarisation (causes receptor to close and repolarise despite receptor still being bound) and blockage of the receptor preventing further depolarisation and muscle contraction.

Uses:

  • Used to relax muscle by blocking activity at the NMJ

Side effects:

  • Initial depolarisation causes fasciculations and increased likelihood of pain on recovery
  • Increase parasympathetic activity:
    • Bradycardia
    • Increased secretion and peristalsis
50
Q

Non-depolarising neuromuscular blockers

Drugs

MoA

Side effects

A
  • Atracurium
  • Vecuronium

Competitive antagonists of Ach receptors preventing depolarisation, blocking the effect of Ach.

Also act presynaptically to reduce Ca2+ entry, reducing its release in vesicles into the synaptic cleft.

3-4 min time to max block, 40-45 min duration.

Side effects:

  • No CNS side effects due to inability to cross BBB
  • Vecuronium has active metabolite that may produce residual paralysis
51
Q

What are the benefits of using non-depolarising neuromuscular blockers instead of depolarising?

A

No CNS effects as they cannot cross the blood-brain barrier

More suitable for LT use than depolarising as show no accumulation effects.

52
Q

What are the potential interactions between inhalational anaesthetics and NMBs?

A

The use of inhalational anaesthetics can increase the action of NMBs

53
Q

Reversal of NMB block

Drugs

MoA

Side effects

A
  • Neostigmine
    • ​Anticholinesterase
    • Reverses the effects of non-polarising NMB but prolongs the effects of polarising NMB suxamethonium.
  • Sugammadex
    • ​Selective relaxant binding agent, binds to the drug to form a complex, encapsulating and inactivating it and preventing it from working at the NMJ.
    • Rapid action, rapidly cleared from plasma and excreted in urine
    • No effect on the cholinergic nervous system, minimises risk of residual paralysis.

Side effects:

  • Neostigmine: bradycardia (due to muscarinic effects on the PNS:
    • ​Atropine or glycopyronium given in conjunction
54
Q

What drugs are used for specific phobias?

A
  • SSRIs: e.g. sertraline
  • B-blockers: e.g. propranolol
55
Q

What drugs are used for panic disorders?

A

SSRIs: e.g. sertraline

56
Q

What drugs are used for PTSD?

A
  • SSRIs e.g. paroxetine
  • Atypical antidepressants: mirtazipine
  • Tricyclic antidepressants: amitryptiline
57
Q

What drugs are used for OCD/body dysmorphic disorders?

A
  • SSRIs e.g sertraline
    • antipsychotic e.g. olanzapine
    • atypical antidepressants e.g. buspirone
58
Q

What drugs are used for short term/crises?

A
  • Benzodiazepines e.g. lorazepam
  • Z-drugs e.g. zolpidem
59
Q

What are the positive and negative aspects of using benzodiazepines for sedation?

A
60
Q

Which opioid receptor do short acting opioids bind to?

A

µ (MOP)

61
Q

Sedatives: Alpha2 adrenergic receptor agonist

Uses

MoA

A
  • Dexmedetomidine

Used as a sedative in intensive care if the patient needs to maintain verbal responsiveness.

By binding to the presynaptic α-2 adrenoceptors in the brain, dexmedetomidine inhibits the release of noradrenaline, and terminates the propagation of pain signals. Activation of the postsynaptic α-2 adrenoceptors inhibits the sympathetic activity, decreasing blood pressure and heart rate.

Drugs List (6 decks)

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