C1 - Addiction Drugs Flashcards
Nitrazepam
A. Benzodiazepine
B. Binds to benzodiazepine1 and 2 receptors activates GABA, increased level of GABA means CNS is inhibited. -> Cl- enters postsynaptic membrane and causes hyper polarization. So slower neurotransmissions in the brain, muscular anxiety and seizures.
C. Insomnia, myoclonic seizures.
Triazolam
A. Sedative/ benzodiazepine (short acting)
B. binds to BDZ1 and 2 receptor, thus activates GABA receptors which causes hyper polarization of postsynaptic membrane, thereby slowing down neuro-excitability.
C. Insomnia
Midazolam
A. Anti-anxiety agent/ benzodiazepine, water soluble (short acting)
B. Binds to several sites in the CNS including the limbic system and reticular formation. Binds to BDZ receptor 1 and 2, thus ncreases membrane permeability to chloride ions by activating GABA. Shift in chloride ions causes hyper polarisation of neuronal membrane.
C. Pre-op sedation, anaesthesia, acute seizures.
Propofol
A. General anaesthetic
B. Short acting lipophillic sedative agent causes global CNS depression agonist action on GABA receptors
C. Anaesthesia
Zolpidem
A. Sedative/ short acting !benzodiazepine analogue!
B. Imidiazopyridine modulates omega 1 receptors (GABA) causes increased chloride conductance leads to hyperpolarisation which inhibits actions potential which decreases neuronal excitability which produces sedative and hypnotic effect.
C. Insomnia
Rucoronium
A. cholinergic R antagonist, amino steroids
B. Non depolarisation skeletal muscle, relaxant, competitive binding to cholinergic nicotinic receptors
C. Tracheal intubation anaesthesia
Sugammadex sodium
A. Acetylcysteine antidote
B. Selective relaxing agent exerts chelating action that encapsulates and terminates amino steroids NMB agent ability to bind to nicotine receptors.
C. Reversal of neuromuscular blockers induced by i.e. Rucoronium
Neostigmine
A. Acetylcholine-esterase inhibitor (peripheral)
B. Competitive inhibitor of cholinesterase resulting in decreased hydrolysis of ACH by ACH-esterase which reduces ACH breakdown increases ACH in the synaptic cleft reverses neurotransmitter blockade.
Doesn’t cross BBB
C. Myasthenia graves (by improving muscle tone)
Morphine hydrochloride
A. Analgesic opioid
B. (Pure opioid agonist selective to muscarinic receptors)
Binds to µ opioid receptors and causes K+ outflow. Leads to hyper polarization, thus no pain transmission (same for all opioids)
C. Acute MI chronic pain
Fentanyl
A. Synthetic opioid, Narcotic agonist-analgesic of opiate receptors
B. Binds to receptors in the brain and spinal cord is reduces pain
agonist to µ opioid receptors and causes K+ outflow. Leads to hyper polarization, thus no pain transmission (same for all opioids)
Leads to analgesia, respiratory depression, sedation
C. Pain relief, surgery premedication, general anaesthesia
Tramadol
A. Synthetic opioid analgesic
B. Opioid synthetic centrally acting analgesic, but may act at least partially by binding to opioid muscarinic receptors causing inhibition of the ascending pathways.
Binds to µ opioid receptors and causes K+ outflow. Leads to hyper polarization, thus no pain transmission (same for all opioids)
C. Severe dental pain.
Burprenorphine
A. Opioid analgesic. semi synthetic, partial opioid
B. Semi synthetic narcotic. Agonist at muscarinic, delta and µ opioid receptors in CNS and antagonistic affects at kappa opioid receptors.
C. Moderate to severe pain, opioid dependance
Naloxone hydrochloride
A. Pure opioid receptor antagonist
B. Produces withdrawal symptoms by competing for opiate receptors sites within CNS
C. Opioid overdose.
Methadoni hydrochloride
A. Synthetic opioid
B. Full U opioid receptor agonist binds to glutametergic NMDA (=glutamate) receptors and acts as an antagonist against glutamate thereby decreases opioid craving and tolerance.
Also binds to µ and lesser to kappa opioid receptors
C. Withdrawal symptoms from opioid, chronic severe pain
Naltrexone hydrochloride
A. Opioid receptor antagonist B. antagonizes µ (kappa, delta) opioid receptors reversible blocks or attenuated the effects of opioid C. Alcohol dependence Opioid management (Naloxonii OD)
Paracetamol
A. Weak COX inhibitor, analgesic, pyretic
B. COX 1, 2 and 3 inhibitor, thus no prostaglandin production. Just centrally acting
C. Fever, minor pain
Metamizole
A. Analgesic
B. Minimal anti inflammatory effects, spasmolytic, pyretic, analgesic
may act on COX an cannabinoid R
C. Fever, painkiller both 2nd line treatment drug
Acamprostate
A. Psychiatric agent
B. Interacts with glutamate (exiting) and GABA (inhibiting), seems to balance them.
Action not fully understood
C. Detox in alcoholism and (renal impairment)
Disulfiram
A. Psychiatry agent
B. Blocks aldehyde dehydrogenase, thus ethanol can’t be metabolized/ oxidized into its end product (acetro acid). degeneration of it stops at acetylaldehyde which is toxic.
(degeneration pathway:
ethanol -> acetylaldehyde -> acetro acid)
Resulting in unpleasant reactions including palpitation hypotension, chest pains and nausea, Vertigo, thirst and nausea
C. Alcoholism
Clonindini hydrochloride
A. Centrally acting alpha2 agonist/ antihypertensives
B. Stimulates alpha2 adrenoreceptors in the brain stem his action results in reduced sympathetic outflow from CNS and decreases peripheral resistance renal vascular resistance and HR BP, may also act on subcortical activity in prefrontal cortex. alters concentration ability and emotions
C. hypertension, ADHD, alcohol detox
