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pharmacology sem 2 > drugs > Flashcards

drugs Flashcards

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1
Q

what is used in the prevention of psycotic episodes?

A

if the person is thought to be at risk of developing psycosis
a. CBT
b. Offer interventions inline with anxiety, depression disorders.
c. Do not give antipsychotics.

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2
Q

what drugs do you give (in order) for psycosis?

A

a. First gen – block D2 receptors
i. Chlorpromazine
ii. Haloperidol
iii. Promazine
b. Second gen- act on a range of receptors + associated with less side effects.
i. Amisulpride
ii. Risperidone
iii. olanzapine
c. Clozapine offered to people who do not respond to two others from the two classes.
d. Depot injections – for maintenance therapy when they do not reliably take oral.
i. Haloperidol
ii. risperidone

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3
Q

how does amisulpride work?

A

selective dopamine receptor antagonist with high affinity for mesolimbic D2 and D3 receptors.

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4
Q

how does chloropromazine work? + whats responsible for its side effects?

A

post-synaptic blockade at the D2 receptors in the mesocortical pathway.
, blocking D2 receptors in the nigrostriatal pathway is responsible for its extrapyramidal side effects
it can also block H1 + M1 receptors

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5
Q

how does clozapine work?

A

Clozapine is a dopamine D1, dopamine D2, 5-HT2A, alpha1-adrenoceptor, and muscarinic-receptor antagonist.

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6
Q

what are the issues with clozapine?

A

its got many dangerous side effects including metabolic syndrome leading to weight gain and type 2 diabetes causing increased lipid levels, seizures and myocarditis

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7
Q

what are the drugs given (in order) for anxiety?

A
  1. SSRI – sertraline or alternative – there’s risks of bleeding particularly for people taking NSAIDs or aspirin – may also consider giving a gastroprotective drug such as omeprazole.
  2. SNRI
  3. Pregabalin
  4. BZDs are only to be used as short term measured of crisis.
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8
Q

what talking therapies are given for MDD?

A

a. CBT
b. behavioural activation
c. group exercise
d. mindfulness and meditation
e. interpersonal psychotherapy
f. Counselling
g. Short term psychodynamic psychotherapy

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9
Q

what pharmacologics are given for MDD?

A

a. SSRIs- sertraline, fluoxetine, citalopram, paroxetine
b. SNRIs- duloxetine, venlafaxine
c. Noradrenaline and specific serotonergic antidepressants – mirtazapine
d. Tricyclic antidepressants – amitriptyline, clomipramine and nortriptyline
e. Serotonin antagonists and reuptake inhibitors – trazodone
f. Monoamine oxidase inhibitors- tranylcypromine, phenelzine

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10
Q

what treatments for treatment-resistant MDD can be given

A

deep brain stimulation
esketamine therapy

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11
Q

how do SSRIs work?

A

they inhibit the reuptake of 5-HT through the SERT receptor allowing more to be available in the synapse allowing it to cause a response through the 5-HTa receptor

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12
Q

how do SNRIs work?

A

they block the reabsorption of 5-HT and NE through the SERT and norepinephrine reuptake receptors, allowing them to bind to NE and 5-HT receptors

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13
Q

what is to be considered when prescribing SNRIs?

A

uncontrolled blood pressure, hepatic imapirment (duloxetine) and renal impairment (duloxetine)

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14
Q

what are some side effects of SNRIs?

A

dry mouth, headache, decreased appetite, nausea, insomnia

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15
Q

what is the long term treatment for bipolar disorder?

A

lithium

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16
Q

how does lithium work?

A

it increases the inhbitory GABA neurotransmitter activity and decreases the stimulatory 5-HT neurotransmission and NMDA receptor activity to act as a mood stabiliser

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17
Q

what are side effects and considerations of lithium?

A

Side effects such as nausea, diarrhoea, tremor and thirst often go away with time, but tiredness, brain fog and weight gain may continue.
regular blood tests to make sure the right amount of lithium in the body

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18
Q

what other mood-stabilising treatments are there?

A

Carbamazepine – if lithium is unsuitable.
Valproate – to treat long term episodes of mania if lithium is unsuitable.
Lamotrigine for severe depression

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19
Q

what is the mechanism of action of sodium valporate?

A

it inhibits Na+ voltage gated channels leading to decreased neuronal excitibility and firing rate, preventing the generation of abnormal electrical impluses for seizures
inhibits GABA transaminase and to inhibit its breakdown, increasing levels of GABA in the brain
enhances GABA synthesis by increasing expression and activity of glutamic acid, respnsible for converting glutamate into GABA
modulates L-type, T-type and N-type Ca2+ channels
inhibits succinate semialdehyde dehydrogenase to lead to a buildup of succinic semialdehyde and imapct GABA metabolism

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20
Q

how does carbmazapine work?

A

modulates voltage gated sodium channels which inhibits action potentials and decreases synaptic transmission, there have been suggestions it keeps sodium channels in their inactive conformations leading to fewer channels opening

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21
Q

how does lamotrigine work?

A

anti-seizure med which selectively binds and inhibits voltage-gated sodium channels, stabilizing presynaptic neuronal membranes and inhibiting presynaptic glutamate and aspartate release
also modulates collapsin response mediator 2 to prevent the formation of abnormal connections in the brain
it can also treat depressive episodes in bipolar

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22
Q

how does mirtazapine work?

A

presynaptic alpha2-adrenoreceptor antagonist which increases central noradrenergic and serotonergic neurotransmission

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23
Q

how does amitriptyline work?

A

its a TCA antidepressant which works by possibly inhibiting the membrane pump responsible for the reuptake of transmitter amines like 5-HT and NE
however, its not reccomended in MDD because of the increased risk of death in overdose

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24
Q

how do mono-amine oxidase inhibitors work?

A

inhibit monoamine-a and/or monoamine b to prevent the breakdown of 5-HT, NE and dopamine (if theyre non-selective)
if theyre selective, the increase dopamine levels through inhibiting monoamine-oxidase B

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25
what are the treatments for alzheimers?
1. Acetyl cholinesterase inhibitors (Donepezil, Galantamine, Rivastigmine) 2. Memantine- glutamate receptor antagonist
26
what are the treatments for parkinsons?
1. Levodopa (dopamine agonist) or monoamine oxidase B inhibitors a. This is where the person is in the initial stages and the motor skills are not impacting their daily life. 2. Monoamine oxidase B inhibitors or catechol-O-methyl transferase inhibitors as an adjunct to levodopa where dyskinesia is impacting their daily life. 3. Non-ergot Dopamine agonist if dyskinesia is still developed after optimal levodopa therapy (pramipexole, ropinirole or rogotine)
27
what cancers have altered expression of EGFR?
- glioblastomas – 54% overexpress wt. and 31% overexpress wt. + EGFRvIII. - non-small cell lung cancers- mutation affecting EGFR exons 18-21= 40-60% of SE Asians - 60-70% response rate in those with sensitising mutations (making TKIs more effective) LREA deletion
28
what types of protein tyrosine kinase mutations are there that make targeted therapies or EGFR antibody treatments effective?
o overexpression/amplification o gain of function mutations o chromosomal rearrangements – brain cancers- kinase domain duplications (EGFR, FGFR3, PDGFRA) o ligand autocrine/ paracrine loop- binds to MET oncogene.
29
what can EGFRvIII mutated tumors not be treated with?
EGFR mAbs as theyre lacking the binding site the Fab fragment needs
30
what makes cancers resistant to TKIs?
binding site mutations Bcl-2 interacting mediator of cell death deletion polymorphism bypassing signalling mutations tumor microenvironment epigentic changes altered metabolism inhibition of cell death through apoptosis, pyroptosis or necrosis
31
what genetic mutations are associated with bypassing signalling of EGFR?
 FGFR  MET  IGF-1R  K-RAS mutation- 15-25% of all lung cancer patients
32
what EGFR antibodies are there?
cetoximab and pantimumab
33
how does cetuximab work?
IgG1 mouse-human mAb which lyses cells by Fc region of the Ab interacting with NK-ADCC +CMC.  1st line EGFR+wtRAS-metastatic colorectal cancer with FOLFOX
34
how does panitumumab work?
IgG2 human mAb which lyses cells by monocyte/macrophage ADCC, 8x the affinity of cetuximab.
35
what must EGFR Abs be combined with?
FOLFOX- fluorouracil, finolic acid and oxaliplatin FOLFIRI- fluorouracil, finolic acid and irinotecan
36
what are type 1 TKIs and how do they work?
gefitinib and erizotinib competitively bind with the ATP binding site on tyrosine kinases to inhbit its phosphorylation and subsequent activation of downstream signalling pathways
37
what are type 2 TKIs and how do they work?
imatinib and sorafenib bind to inactive ATP binding site on tyrosine kinases
38
what are type 4 and 5 TKIs and how do they work?
osmertinib and afatinib osmertinib was designed to overcome resistance from the T790M and is now a first line treatment for NSCLC they irreversibly bind to kinase sites and have better pharmacokenetics than the reversible ones
39
what is pyrosinib?
its a multi-action tyrosine kinase inhibitor aimed at inhibiting EGFR, HER2 and HER4 its known as a pan-Erb-receptor tyrosine kinase inhibitor used in metasatic breast cancer
40
what are KRAS inhibitors?
sotoasib and adagrasib targets one of the main mutations found in non-small cell lung cancer (KRAS G12C mutation) it inhibits the RAD-GTPase family for targeted anti-cancer effects on specific mutated cancers
41
when are KRAS inhibitors used?
when attempts to treat the cancer with platinum-based chemo, or anti-PD-1/PD-L1 immunotherapy havent been successful
42
what other small molecule inibitors are there for the treatment of cancer?
- BRAF inhibitors target the altered BRAF protein allowing cells to grow. - MEK inhibitors target the altered MEK proteins which allow the cells to grow. nivolumab - PD-1 inhibitor regorafenib - multi-target tyrosine kinase
43
what is the fact about glioblastomas and TKIs?
TKIs can activate general control non-depressible 2 (GCND2) to phosphorylate ELF2alpha to activate AFT4 genes for cell stress response and amino acid depravation, along with inhibiting protein synthesis to result in cell death tang et al 2022
44
what are the side effects of tyrosine kinase inhibitors?
the main ones are a rash (grade 3/4 in 10% of patients) and diarhoea (grade 3/4 in 6% of patients)
45
what are the genetic indicators of TKIs being effective or ineffective treatments in cancers?
EGFR mutations indicate that the treatment will be effective and KRAS mutations indicate that theyll be ineffective
46
what treatments other than the normal ones for gliomas are there?
anti-VEGF-A- bevacizumab EGFR Abs - however these are less effective in the brain as the mutations are in the extracellular domain rather than the kinase domain like non-small-cell lung cancers regorafinib - multitarget tyrosine kinase inhibitor
47
how does regorafinib work?
its a multi-target tyrosine kinase inhibitor targeting VEGFR1-3 + TIE2 (genes involved in angiogenesis), KET, RET, RAF1 + BRAF (genes involved in oncogenesis), PDGFR+ FBDGFR (TME) and CSF1R (tumor immunity) the overall 1yr survival was 39%
48
what are the treatments for status epilicticus?
midazolam (buccal) or diazepam (rectal) or IV lorazepam if access to IVs
49
what treatments are there for focal seizures?
1. lamotrigine or levetiracetam 2. carbamazepine or oxcarbazepine
50
what are the treatments for absense seizures?
1. ethosuximide 2. sodium valproate
51
what are the treatments for myoclonic seizures?
1. sodium valproate 2. levetiracetam they occur in a variety of symptoms and the responses to treatments vary
52
what are the treatments for atomic or tonic seizures?
1. sodium valproate 2. lamotrigine these are usually seen in children and are associated with cerebral damage
53
what treatments are there for dravet syndrome?
sodium valporate regardless of women of childbearing age because of the severity of symptoms
54
what are the risks associated with sodium valporate?
highly teratogenic and leads to 10% risk of congenital malformations and 30-40% risk of neurodevelopmental disorders.
55
whats the mechanism of action of ethoxumide?
it inhibits T type Ca2+ channels (the low lotage activated channels_ 1st line for absence seizures
56
whats the mechanism of action of levetiracetam?
unclear moa but seems to bind to synaptic vesicle protein 2 which is part of secretory vesicles which mediate the Ca2+ dependant vesicular neurotransmitter release to decrease the rate of vesicle release
57
what other treatments can be used for treatment resistant status epilicticus?
ketamine has been said to be effective in super refractory status epilepticus with at least 50% decrease in seizure activity within the first 24hrs
58
what is the mechanism of action for pregabalin and gabapentin?
they both inhibit the alpha 2 subunit of the Ca2+ channel (the HVA Ca2+ channel)
59
what are the consequences of status epilicticus?
it can result in prolonged seizure activity leading to neuronal injury/ death or alter neuronal networks leading to long term cognitive deficits
60
what are some of the causes of seizures?
temperature stroke overdose hypoglycemic episodes dementia dravet syndrome infection (meningitus) glutamate-GLUT-1-transporter deficiency autism
61
what type of focal seizures are there?
aura motor autonomic awareness the main treatment for them is lamotrigine or lascosamide which are voltage gated Na+ channel inhibitors
62
what is the novel treatment of schizophrenia?
KartX which inhbits M1-5 peripherally by tropsium and agonises M1 and M4 in the CNS to target the positive and negative symptoms with xanthomline this increases the safety profile of the drug and reduces the side effects it also increases dopamine release in the PFC and hippocampus and decreases dopamine release in the substantia nirgra, ventral striatum and neuclus accumbens
63
what parts of MDD act on the volume transmission and which ones act on synaptic transmission?
the monoamines target the volume transmission, having wide impacting effects and glutamate acts on the synaptic transmission, acting on the NMDA receptors for excitatory effects on the neurons
64
what is the pathophysiology reasons for seizures?
its thought that imbalances between glutamate and GABA stimulate neurotransmission and overexitation of the neurons causing seizures
65
what impact do BZDs have on cloride ion channels opening?
they increase the frequancy of the chloride ion channels opening, allowing repolarisation of the cell and inhibition of the signal
66

pharmacology sem 2 (5 decks)

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