C1 - Addiction Drugs

Question 1

Nitrazepam

Answer 1

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.

Question 2

Triazolam

Answer 2

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

Question 3

Midazolam

Answer 3

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.

Question 3

Propofol

Answer 3

A. General anaesthetic
B. Short acting lipophillic sedative agent causes global CNS depression agonist action on GABA receptors
C. Anaesthesia

Question 4

Zolpidem

Answer 4

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

Question 6

Rucoronium

Answer 6

A. cholinergic R antagonist, amino steroids
B. Non depolarisation skeletal muscle, relaxant, competitive binding to cholinergic nicotinic receptors
C. Tracheal intubation anaesthesia

Question 7

Sugammadex sodium

Answer 7

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

Question 8

Neostigmine

Answer 8

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)

Question 9

Morphine hydrochloride

Answer 9

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

Question 10

Fentanyl

Answer 10

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

Question 11

Tramadol

Answer 11

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.

Question 12

Burprenorphine

Answer 12

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

Question 12

Naloxone hydrochloride

Answer 12

A. Pure opioid receptor antagonist
B. Produces withdrawal symptoms by competing for opiate receptors sites within CNS
C. Opioid overdose.

Question 13

Methadoni hydrochloride

Answer 13

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

Question 15

Naltrexone hydrochloride

Answer 15

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)

Question 16

Paracetamol

Answer 16

A. Weak COX inhibitor, analgesic, pyretic
B. COX 1, 2 and 3 inhibitor, thus no prostaglandin production. Just centrally acting
C. Fever, minor pain

Question 17

Metamizole

Answer 17

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

Question 18

Acamprostate

Answer 18

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)

Question 19

Disulfiram

Answer 19

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

Question 20

Clonindini hydrochloride

Answer 20

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