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Sem 3 > pharmacology > Flashcards

pharmacology Flashcards

1
Q

When do we used sodium valproate?

A
  1. epilepsy (anti convulsion)

2. bipolar disorder (acute disorders and prophylaxis): mood stabiliser

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2
Q

What is the mechanism of action of sodium valproate?

A
  1. weak inhibitor of neuronal voltage gated NA+: stabilises resting membrane potentials and reduces neuronal excitability
  2. GABAergic: inhibits GABA transaminase (increases GABA concentration at receptor sites)
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3
Q

What are the side effects of sodium valproate?

A

nausea, dyspepsia, weight gain, hepatic and renal impairment, dizziness, drowsiness, thrombocytopenia, hair loss

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4
Q

What are the problems with using valproate sodium during pregnancy?

A

folate antagonist properties: inhibits the DHFR protein (enzyme used to activate folic acid and before it enters folate metabolism cycle)

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5
Q

What is the mechanism of action of lithium?

A

increase GABA

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6
Q

When do you use Gabapentin?

A
  1. epilepsy ( anticonvulsant): usually as an add on treatment if other epileptic drugs provide inadequate control
  2. Neuropathic pain
  3. Migraine prophylaxis
  4. GAD
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7
Q

What is the mechanism of action of gabapentin?

A

reduction of axon excitability:
acts on voltage sensitive calcium channels (binds to alpha-2 delta subunits): prevents inflow of calcium which inhibits neurotransmitter release (glutamate, noradrenaline and substance P)

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8
Q

What are side effects of gabapentin?

A

somnolence, dizziness, ataxia, fatigue

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9
Q

When do you use tricyclic antidepressants?

A
  1. moderate to severe depression (when first line SSRIs are ineffective)
    (2. anxiety)
  2. neuropathic pain
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10
Q

What are the side effects of tricyclic antidepressants?

A
  1. antimuscarinic receptors: dry mouth & nose, constipation, urinary retention and blurred vision
  2. histamine and adrenergic receptors: sedation, hypotension
  3. arrhythmia,ECG changes
  4. convulsions, hallucination and mania

DON’T STOP THEM SUDDENLY

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11
Q

What are the mechanism of actions of tricyclic antidepressants?

A
  1. inhibits presynaptic 5-HT and NA reuptake transporters: increase synaptic neurotransmitter availability (monoamine theory of depression)
  2. analgesic mechanism unknown: thought to result from modulation of inhibitory systems and opioid systems in CNS
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12
Q

When do you use lidocaine?

A
  1. local anaesthesia

2. ventricular arrhythmias

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13
Q

What is the mechanism of action of lidocaine?

A

Blockage of fast voltage-gated NA+ channels in neuronal membrane: prevents depolarisation along axon (propagation)

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14
Q

What are the side effects of lidocaine?

A
  • dizziness/drowsiness

- paraesthesia

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15
Q

When do you use paracetamol?

A
  • analgesic effects in acute and chronic pain

- reduce fever: antipyretic effects

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16
Q

What is the mechanism of action of paracetamol?

A

increases pain threshold in CNS by inhibiting COX (cyclooxyrgenase)

  1. reduces prostaglandin PGE2 concentration in thermoregulatory region of hypothalamus
  2. COX 2 inhibition: reduces inflammation (weak anti-inflammatory)
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17
Q

What are the SE of paracetamol?

A

in overdose: liver failure

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18
Q

When do you use ibuprofen?

A
  1. analgesia (mild to moderate pain)
  2. anti-inflammatory
    (3. antipyretic)
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19
Q

What is the mechanism of action of ibuprofen?

A

-inhibition of COX2: prevents prostaglandin formation from arachidonic acid
(COX2 is expressed in response to inflammatory stimuli–> causes pain)

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20
Q

What are the SE of ibuprofen?

A
  • -> due to COX1 inhibition:
  • nausea and dyspepsia
  • GI ulceration/bleeding
  • risk of hypertension in chronic use
  • cardiovascular event
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21
Q

When do you use morphine?

A
  • acute severe pain
  • chronic pain
  • breathlessness (in end of life care)
  • acute pulmonary oedema (breathlessness and anxiety)
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22
Q

What is the MOA of morphine?

A

Activation of mu receptors (G protein-coupled receptors) in CNS

  • -> reduces neuronal excitability (post-synaptic opioid receptor activation causing hyper polarisation) recent and pain transmission (activation of pre-synaptic opioid receptors: reduced intracellular cAMP C°, decreased Ca ion influx and thus inhibits release of excitatory neurotransmitters)
  • -> in medulla: blunt response to hypoxia and hypercapnoea (reduces rest drive and breathlessness)
  • -> reduces fight or flight activity (by reducing pain, breathlessness and associated anxiety)

(also acts on GABA neurones that modulate dopamine: by inhibition GABA you are able to increase dopamine)

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23
Q

What are the SE of morphine?

A
  • respiratory depression (by reducing respiratory drive)
  • euphoria and detachment/ neurological depression
  • nausea and vomiting (activa° of chemoreceptors trigger zone)
  • pupillary constriction (stimulation of E-W nucleus)
  • constipation (increase smooth muscle tone and reduces motility)
  • skin itching (histamine release)
  • -> tolerance, dependence, withdrawal reaction
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24
Q

What is co-codamol?

A

codeine and paracetamol

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25
Q

When do you use co-codamol?

A

mild to moderate pain, as a second line treatment when simple analgesics are insufficient

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26
Q

What is the MOA of co-codamol?

A
  • mechanism of paracetamol

- metabolised by cytochrome P450 enzymes to morphine (or morphine related metabolites)

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27
Q

What are the SE of co-codamol?

A
  • at recommended dose, SE from paracetamol are rare

- codeine: nauseas, constipation and drowsiness

28
Q

When do you use aspirin?

A
  1. acute coronary syndrome an acute ischemic stroke
  2. long term secondary prevention in cardiovascular, cerebrovascular and peripheral arterial disease
  3. atrial fibrillation (if warfarin and oral anticoagulants are contraindicated)
  4. control mild to moderate fever and pain
29
Q

What is the MOA of aspirin?

A

Irreversible inhibition of COX to reduce production of pro-aggregators factor thromboxane from arachidonic acid, reducing platelet aggregation

30
Q

What are the SE of aspirin?

A
  • gastrointestinal irritation and ulceration
  • haemorrhage
  • bronchospasm
  • life threatening in overdose
31
Q

What type of drug is diazepam?

A

benzodiazepines

32
Q

When do you use benzodiazepines?

A
  • seizures (first line)
  • alcohol withdrawal reactions
  • severe, disabling or distressing anxiety or insomnia (short term treatment)
33
Q

What inhibits benzodiazepines? how?

A

flumazenil

displaces diazepam from GABA receptor

34
Q

What is the MOA of benzodiazepines?

A
  • positive allosteric modulator (POM): facilitate and enhance binding of GABA to GABA-A receptor (between alpha and gamma subunits): depressant effect on synaptic transmission (hyperpolarisation)
  • -> effects: sleepiness, reduces anxiety, sedation and anticonvulsant effects
35
Q

What are the SE of benzodiazepines?

A
  • dose dependent drowsiness, sedation and coma
  • loss of airway reflexes (airway obstruction and death)
  • dependence, withdrawal reaction
36
Q

Name an SSRI?

A

sertraline

37
Q

When do you use SSRIs?

A
  • moderate to severe depression (first line treatment BUT only if psychological treatments fail
  • panic disorders
  • obsessive compulsive disorder
38
Q

What is the MOA of SSRIs?

A

inhibit neuronal re-uptake of serotonin from the synaptic cleft: increase availability for neurotransmission

39
Q

What are the SE of SSRIs?

A
  • gastrointestinal upset, appetite and weight disturbance (loss or gain) an hypersensitivity reactions
  • suicidal thoughts and behaviour
  • -> sudden withdrawal may cause problems
40
Q

Name an SNRI

A

venlaxafine

41
Q

What does SSRI stand for?

A

selective serotonin reuptake inhibitor

42
Q

What does SNRI stand for?

A

serotonin and norepinephrine reuptake inhibitors

43
Q

When do we use SNRIs?

A
  • second line treatment for MDD

- general anxiety disorder

44
Q

What is the MOA of SNRIs?

A

-serotonin and noradrenaline reuptake inhibitor (from synaptic cleft)

45
Q

What are the SE of SNRIs?

A
  • gastrointestinal upset
  • CNS effect (abnormal dreams, insomnia, headache, convulsion etc)
  • suicidal thoughts
  • -> sudden withdrawal causes big effects
46
Q

What is in co-beneldopa?

A
  • levadopa (L-DOPA)
  • peripheral dopa-decarboxylase inhibitor
  • -> reduces conversion to dopamine outside the brain
47
Q

When do you use co-beneldopa?

A

parkinson’s disease

48
Q

What is the MOA of co-beneldopa?

A

precursor of dopamine (L-DOPA) which can cross the BBB via membrane transporters and then be converted into dopamine

49
Q

What are the SE of Co-beneldopa?

A
  • nausea, drowsiness, confusion, hallucinations and hypotension
  • wearing off effect
  • dyskinesias (on-off effect: phases of immobility and phases of dyskinesias)
50
Q

Name a MAO-B inhibitor

A

selegiline

51
Q

what does MAO-B stand for?

A

monoamine oxidase type B

52
Q

When are MAO-B inhibitors used?

A

Parkinson’s disease

53
Q

When are MAO-A inhibitors used?

A

depression

54
Q

What is the MOA of MAO-B inhibitors?

A

inhibition of MAO-B which metabolises dopamine and phenylethylamine, increasing available dopamine
+enhances effects of L-DOPA

55
Q

What are the Se of MAO-B inhibitors?

A
  • dizziness, nausea, fatigue
  • possible hyper sexuality or similar behaviour (due to increased dopamine)
  • can cause worsening of levodopa induced dyskinesia
  • sometimes hallucinations
56
Q

Name two second generation (atypical) antipsychotic

A

clozapine and risperidone

57
Q

When do we use second generation (atypical) antipsychotics?

A
  • psychomotor agitation (urgent treatment)
  • schizophrenia
  • bipolar disorder (in episodes of mania or hypomania)
58
Q

What are the SE of second generation (atypical) antipsychotics?

A
  • sedation
  • EPSE (ie Parkinsonism)
  • metabolic disturbances
  • arrhythmias
  • agrunolocytosis
59
Q

Which nerve fibres are more sensitive to local anaesthetics?

A

small nerve fibre> large nerve fibres

myelinated fibres> non myelinated fibres

60
Q

when using an anaesthetics, which are the order of loss of nerve functions?

A

pain, temperature, touch, proprioception and finally skeletal muscle tone

61
Q

Why is ketamine used in surgery?

A

-reduces incidence of post surgical pain

62
Q

What is an adjuvant?

A

enhancing the effectiveness of medical treatment

63
Q

what are examples of adjuvants in pain management?

A
  • gabapentin/pregabapentin
  • SNRIs/ tryclic antidepressants
  • alpha2agonists
64
Q

what is the MOA of cannabis?

A

activation of presynaptic CB1 receptors (G coupled receptors) in the hypothalamus, sustantia nigra,mesolimbic pathways and association areas of the cerebral cortex
–> causes inhibition of voltage gated Ca channels: reducing transmitter release

65
Q

when is propofol used?

How is given?

A
  • hypnosis

- bolus: fast acting but short acting

66
Q

What is isoflurane used? How is given?

A
  • hypnosis

- inhalant gas

Sem 3 (20 decks)

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