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DRUGS SEM 3 > from all cases > Flashcards

from all cases Flashcards

1
Q

what is depakote? uses?

A
  • valproate semisodium (valproic acid and sodium valproate)
  • antiepileptic
  • effective in bipolar disorder and in the prevention of migraine headaches
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2
Q

depakote MoA acute effects

A
  • increases GABA
  • decreases neuronal excitability via the blockage of voltage gated Na+ channels
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3
Q

depakote longer-term effects

A

changes in:
- glucocorticoid, 5-HT and DA neurotransmitter systems
- inositol metabolism and protein kinase C activity
- Wnt/B-catenin cell signalling pathway
- brain lipids and their metabolism

  • increased trophic and protecting facets eg. BDNF and the anti-apoptosis factor B-cell lymphoma-2 (Bcl-2)
  • class 1 his tone deacetylases (HDAC) inhibition —> altered gene expression
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4
Q

valproate side effects

A
  • LOTS
  • very common - nausea, tremor, weight gain
  • increases risk of spina bifida x12-16 in pregnant women, also increased risk of cleft palate, autism, postnatal neurodevelopmental problems, atrial septal defect etc
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5
Q

paracetamol use and MoA

A
  • effective analgesic for acute pain
  • COX inhibitor
  • inhibits prostaglandin synthesis by reducing COX1 and COX2
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6
Q

wha can acute paracetamol overdose lead to?

A

fatal liver damage

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7
Q

ibuprofen MoA and SEs

A
  • NSAID — reduce tissue inflammation and nociception
  • non-selective, reversible inhibition of COX1 and COX2
  • reduce prostaglandin synthesis via the arachidonic acid pathway
  • the inhibition of COX1 is thought to cause some of the side effects such as GI ulceration
  • GI ulceration, GI irritation, renal toxicity, some cardiovascular side effects such as MI and hypertension
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8
Q

gabapentin and pregabalin MoA and SEs

A
  • anticonvulsants used in pain management
  • binds to a2d part of Ca channel — decreases subsequent release of excitatory neurotransmitters such as glu, substance P, NE and CGRP
  • dizziness, sleepiness, water retention, difficulty walking, upset stomach
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9
Q

tricyclic antidepressant example

A

amitriptyline

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10
Q

tricyclic antidepressant use MoA

A
  • analgesic and treatment of depression and anxiety-related disorders (used in treatment resistant cases)
  • act at presynaptic 5-HT and NA reuptake transporters, increasing the availability of these neurotransmitters
  • also block postsynaptic histamine and muscarinic-ACh receptos contributing to many of their side effects

BLOCK SERT AND NAT

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11
Q

amitriptyline side effects

A

dry mouth, constipation, dizziness, sleepiness, headache, difficulty peeinhg, weight gain, memory impairment

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12
Q

codeine use and MoA

A
  • codeine is an opioid analgesic used to treat moderate to severe pain
  • selective for the mu opioid receptor
  • opioids reduce pain signal transmission by activating post-synaptic opioid receptors — leads to reduced intracellular cAMP conc, decreased Ca++ influx and thus inhibits the release of several neurotransmitters such as glutamate and substance P
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13
Q

lidocaine MoA

A

blockage of Na+ channels prevents depolarisation along axons, thus preventing signal propagation

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14
Q

alteplase uses and MoA

A
  • tissue plasminogen activator
  • used in stroke — intravenous thrombolysis
  • aims to dissolve the thrombus to allow reperfusion
  • catalyses the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown
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15
Q

aspirin MoA

A
  • inhibits cyclo-oxygenase, which converts arachidonic acid to prostaglandins and thromboxanes
  • thromboxane, under normal circumstances, binds platelet molecules together to create a patch over damaged walls of blood vessels. this platelet clump can become too large and block blood flow
  • aspirin, an anti-thrombotic drug, is an immediate treatment after an ischaemic stroke to reduce the likelihood of having another stroke
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16
Q

diazepam uses and MoA

A
  • acts on GABA (A) receptor
  • allosteric modulator at GABA receptors
  • GABA binds between alpha and beta subunits causing Cl- to flow into neurone and hyperpolarise cell — major inhibitory neurotransmitter and is present in 30% of brain synapses
  • diazepam binds at separate site between alpha and gamma subunits — this potentiates the action of GABA and increase Cl- influx
  • eases anxiety within 0.5-1 hours
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17
Q

name some SSRIs

A

sertraline, paroxetine, escitalopram, fluoxetine

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18
Q

SSRIs MoA

A
  • block serotonin (5-HT) reuptake from synapse
  • increases amount of 5-HT in synaptic cleft
  • not addictive, may take 1-2 weeks to start working, effective in 70% of cases
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19
Q

common side effects of SSRIs

A

nausea, dry mouth, low sex drive, blurred vision, dizziness, loss of appetite, insomnia, sweating

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20
Q

common side effects of diazepam

A

sedation, respiratory depression, tolerance, dependence, impaired cognition
- shouldn’t be prescribed for more than 4 weeks

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21
Q

statin MoA

A
  • eg. atorvastatin
  • competitively inhibit HMG-CoA reductase = rate limiting enzyme in the production of cholesterol in the liver
  • reduces liver production of cholesterol —> leads to more LDL receptors
  • increased removal of LDL from plasma
  • also increase HDL and lower triglycerides
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22
Q

side effects of statins

A

myosotis, rhabdomyolysis (rapid breakdown of skeletal muscle — causes dark coloured urine — myoglobin released from muscle and ends up in urine — toxic for kidneys — kidney failure), altered liver function tests, complications are rare but lots of people are taking them

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23
Q

what do tricyclic, SSRI and SNRI antidepressants block?

A

SERT and/or NAT — increase synaptic levels of 5-HT and/or NA

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24
Q

patients on an MAO must stick to what kind of diet?

A

low tyramine (or could lead to a hypertensive crisis and stroke)

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25
Q

MAO-A vs MAO-B inhibitors use

A

MAO-A = antidepressants
MAO-B = parkinson’s

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26
Q

name 2 SNRIs

A

venlafaxine and duloxetine

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27
Q

why are SSRIs safer in overdose than tricyclics?

A

Like tricyclics these drugs block both reuptake transporters. However, they lack the unwanted binding at a range of receptors that the tricyclics generally have and therefore tend to have fewer side effects and are safer in overdose.

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28
Q

newer antidepressant MoA : mirtazapine

A
  1. principally an adrenergic a2 receptor antagonist
  2. noradrenergic a2R antagonism blocks the -ve feedback whcih is tending to reduce NA release
  3. net effect is increased NA release
  4. noradrenergic a2R antagonism also blocks the -ve feedback,c tending to reduce 5-HT release. net effect is increased 5-HT release
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29
Q

main drug is MS treatment

A

methylprednisolone

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30
Q

glatiramer acetate use and MoA

A
  • preventing MS relapse
  • structurally similar to myelin-basic protein
  • binds to T lymphocytes and blocs the presentation of myelin antigens to the T cells
  • given IV
31
Q

B-interferon use and MoA

A
  • preventing MS relapses
  • can be given by self injection in trained patients
  • causes down regulation of interferon-y and increases the activity of suppressor T cells
  • treatment of relapsing-remitting MS
  • bind to type 1 interferon receptos
  • binding changes expression of immunomodaltor proteins in the brain, reducing inflammatory processes
32
Q

natalizumab use and MoA

A
  • reducing MS relapses
  • prevents lymphocyte migration across BBB
33
Q

side effect of natalizumab

A

progressive multi focal leukocephelopathy (PML) — caused by JC virus, 50% of population have positive antibodies, virus stays latent in various organs including kidneys, lungs, spleen, bone marrow, B cells and tonsils

34
Q

name a benzodiazepine

A

diazepam

35
Q

levadopa use and MoA

A
  • 1st line PD treatment
  • can cross BBB unlike DA
  • very short acting
  • decarboxylated to DA
  • taken with food to avoid nausea vomiting
    = directly increases DA levels in brain
36
Q

side effects of levodopa

A
  • dyskinesias
  • compulsive behaviour
  • psychosis
37
Q

why does the effectiveness of levodopa gradually decline over time?

A

—> this mainly reflects the natural progression of the disease, but receptor downregulation and other compensatory mechanisms also contribute. the ability of neurones to store dopamine is lost to the therapeutic benefit of levodopa depends increasingly on the contrinous formation of extranueronal dopamine

38
Q

what is levadopa normally given with?

A

carbidopa (cocardopa), entacapone or benserazide (cobeneldopa)— agents that decrease L-dopa metabolism and thus prolong its half life

39
Q

benserazide MoA

A
  • a peripherally-acting DOPA decarboxylase inhibitor
  • combined with levodopa to reduce peripheral side effects
  • cannot cross the BBB so doesn’t prevent the effects of levodopa in the brain
40
Q

what is co-beneldopa?

A

levodopa and benserazide

41
Q

rasagiline and selegiline MoA and use

A
  • MAO-B inhibitors
  • inhibition of MAO-B protects dopamine from extraneuronal degradation
  • MAO-B preferentially metabolises dopamine over NE and 5-HT
  • adjunctive to levodopa
  • may enhance adverse effects of L-dopa
  • no cheese-effect (acute attack of hypertension that can occur in a person taking a MAOI drug who eats cheese due to the interaction of MAOI width tyramine)
42
Q

entacapone MoA and use

A
  • COMT inhibitor
  • COMT break downs dopamine, adrenaline and noradrenaline
  • prevents peripheral breakdown of levodopa, allowing more levadopa to reach the brain
43
Q

what are used in 1st line treatment of schizophrenia?

A

2nd generation antipsychotics = risperidone, olanzapine, quetiapine, aripiprazole

44
Q

name a 1st generation AP

A

haloperidol

45
Q

what is used in treatment resistant Sz?

A

clozapine

46
Q

how do all known antipsychotics work?

A

reduce positive symptoms by blocking true D2 receptors in the associative striatum ie. they are D2 receptor antagonists
- many also block the D3 D4 receptor and 5-HT2A receptors, but that doesnt reduce antipsychotic symptoms

47
Q

for antipsychotic efficacy, a drug must block more than what % of D2 receptors in the associative striatum?

A

65%

48
Q

antipsychotics SEs

A
49
Q

what is used for treatment resistant Sz (TRS)?

A

clozapine

50
Q

why is clozapine a ‘dirty drug’?

A

lots of side effects

  • sedation
  • hunger
  • hypersalviaiton
  • diabetes
  • rare : agranulocytosis
51
Q

what does clozapine bind best to?

A

D4

52
Q

suxamethonium MoA and use

A
  • depolarising neuromuscular blocking agent
  • muscle relaxant — intubation
  • persistent depolarisation of NMJ by mimicking the effect of ACh without being rapidly hydrolysed by acetylcholinesterase. constant depolarisation leads to desensitisation
53
Q

atracurium MoA and use

A
  • non-depolarising neuromuscular blocking agent
  • competitive antagonist at the ACH receptors of the motor endplate
  • cause motor paralysis —> help facilitate endotracheal intubation
54
Q

major SEs of non-depolarising blockers

A

hypotension, bronchospasm (due to histamine release), wheeze, tachycardia or bradycardia anaphylaxis, incomplete reversal

55
Q

major SEs of depolarising neuromuscular blocking agents

A

muscle pain, hyperkalaemia, malignant hyperthermia, anaphylaxis, suxamethonium apnoea, increased intracranial/ocular pressure (due to muscle twitching)

56
Q

neostigmine use and MoA

A
  • used to reverse effects of muscle relaxants
  • blocks acetylcholinesterase — increases ACh conc in NMJ
57
Q

atropine/glycopyrrolate use and MoA

A
  • used to limit the parasympathetic effects of neostigmine eg. bradycardia
  • competitive antagonist at muscarinic receptor
58
Q

atropine vs glycopyrrolate

A

atropine can cross the BBB

59
Q

fentanyl use and MoA

A
  • potent narcotic analgesic

strong agonist at the mu opioid receptor. upon binding, GTP —> GDP on the G-proteins which in turn down regulates adenylate cyclase, reducing cAMP concentrations —> reduced Ca++ influx in to cell —> hyperpolarisation of cell and inhibition of nerve activity

When fentanyl binds, downstream signaling leads to the inhibitory effects, such as decreased cAMP production, decreased calcium ion influx, and increased potassium efflux.[56] This inhibits the ascending pathways in the central nervous system to increase pain threshold by changing the perception of pain; this is mediated by decreasing propagation of nociceptive signals, resulting in analgesic effects
adenylate cyclase inhibition —> deceased release of nociceptive substacens such as substance P, GABA, DA etc

60
Q

propofol use and MoA

A
  • iv induction of general anaesthesia and can be given as continuous infusion to maintain anaesthesia
    —> positive modulation of GABA through GABA-A receptor — cause an increased influx of Cl- ions into the post synaptic neuron
    (GABA-A receptors are ligand-gated ion channles (Ionotropic receptors) - most abundant fast inhibitory neurotransmitter receptors of the CNS. anaesthetics mainly work in extrasynapotic GABA-A receptors)
61
Q

isoflurane use and MoA

A
  • inhalation inducing agent and maintenance of general anaesthesia

: likely binds to GABA, NMDA (glutamates) and glycine receptors. NOT UNDERSTOOD

62
Q

what irreversibly blocks VMAT?

A

reserpine

63
Q

what drugs are effective for acute mania?

A
  • all antipsychotics (D2 receptor antagonists)
  • lithium (mood stabiliser)
  • valproate (antiepileptic)
  • carbamazepine (antiepileptic)
64
Q

what are the effects of lithium?

A
  • increase in 5-HT and GABA neurotransmission
  • decrease in Glu and DA neurotransmission
  • decrease in oxidative stress
  • increase in trophic and protective factors eg BDNF and Hcl-2
65
Q

what is a GABA analogue which acts as a selective agonist at GABAB receptors, used clinically as a muscle relaxant?

A

baclofen

66
Q

who do benzodiazepines work?

A

bind at a separate site between the a and y subunits on GABAAR — this potentiates the action of GABA and increases Cl- influx

ie. it is a positive allosteric modulator (POM) at the GABAA receptor

67
Q

name some MAOIs

A
  • irreversible = phenelzine, tranylcypromine
  • reversible = moclobomide
68
Q

what are imipramine, desipramine, amitriptyline, clomipramine?

A

tricyclic antidepressants

69
Q

treatment of tic disorders

A
70
Q

what does amantadine do?

A

blocks glutamatergic NMDAR in basal ganglia

71
Q

name 2 COMT inhibitors

A

entacapone and tolcapone

72
Q

treatment of dyskinesias

A
  1. amantadine — NMDAR antagonist — blocks Glu — reduces dyskinesias by about 40%
  2. continuous dopaminergic stimulation— apomorphine (DA agonist by iv) or duodopa (into intestine) — fewer fluctuations
73
Q

describe the actions and uses of benserazide, entacapone, and carbidopa

A

—> prescribed with L-DOPA to prevent its peripheral breakdown, so more can reach the brain

  1. benserazide — L-DOPA decarboxylase inhibitor
  2. carbidopa — L-DOPA decarboxylase inhibitor
  3. entacapone — COMT inhibitor
74
Q

Myasthenia gravis medication

A

medications such as Pyridostigmine — inhibitor of AChE — prevent the breakdown of ACh — increase synaptic availability of ACh

these medicines tend to work best in cases of mild myasthenia gravis. they can improve muscle contractions and strength in the affected muscles

DRUGS SEM 3 (1 decks)

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