- •Simplicified version! Drugs Affecting the Afferent Innervation
- •Indications:
- •Indications 3 - 6
- •Indication 1
- •Indication 2
- •Indications:
- •(CholinOnegative drugs)
- •Anticholinesterases
- •Muscarinic agonists (m-cholinomimetics)
- •Nicotinic agonists (n-cholinomimetics)
- •Simplicified version
- •(Cholinonegative drugs)
- •Muscarinic antagonists (m-cholinoblockers)
- •Nicotinic antagonists (n-cholinoblockers)
- •Ganglion-blocking drugs
- •Neuromuscular blocking drugs (myorelaxants)
- •Simplicified version
- •(Adrenopositive drugs)
- •Indirect adrenomimetics
- •Direct adrenomimetics
- •Mixed action Adrenomimetics
- •Alfa-adrenomimetics
- •Beta-adrenomimetics
- •Simplicified version
- •(Adrenonegative drugs)
- •Sympatholytics
- •Alfa-adrenoblockers
- •Beta-adrenoblockers
- •General anesthetics
- •Analgesic drugs
- •Hypnotic drugs
- •Antiepileptic drugs (anticonvulsants)
- •Sedative drugs
- •Anxyolytics (antianxiety drugs, tranquillizers)
- •Antipsychotic drugs (neuroleptics)
- •Analeptics
Analgesic drugs
List of drugs
Opioid (narcotic) analgesics: Morphine hydrochloride, Trimeperidine, Fentanyl
Non-opioid (non-narcotic) analgesics: Acetylsalicylic acid, Paracetamol (Acetaminophen), Metamizole
Mechanism of action
Opioid (narcotic) analgesics produce stimulation of -opioid receptors ( = “mu”).
Non-opioid analgesics produce inhibition of cyclooxygenase type 1 (COX-1) and, as result, impairment of prostaglandin synthesis.
Pharmacological effects
Opioid and non-opioid analgesics decrease the pain by blocking of the transmission of pain stimuli in the central nervous system without influencing all another types of sensation (tactile sense etc.)
Indications
Traumatic pain (any opioid analgesics)
Opioid analgesics → stimulation of -opioid receptors → blockage of the transmission of pain stimuli in the central nervous system→ pain relieving.
Ischemic pain (any opioid analgesics, but more preferable is Fentanyl due to the most strong painkilling activity)
Opioid analgesics → stimulation of -opioid receptors → blockage of the transmission of pain stimuli in the central nervous system→ pain relieving.
Inflammatory pain (e.g. toothache, headache etc.) (any non-opioid analgesics)
Non-opioid analgesics → inhibition of COX-1 and, as result, impairment of prostaglandin synthesis → blockage of the transmission of pain stimuli in the central nervous system→ pain relieving.
Side effects:
Morphine hydrochloride and Fentanyl can produce inhibition of respiratory center.
Non-opioid analgesics can produce the damage of gastric mucosa (gastritis, ulcer disease).
NB! In case of overdosage of opioid analgesics we should use Naloxone hydrochloride which produces the blockage of -opioid receptors and thus inhibits the activity of opioid analgesics.
Hypnotic drugs
List of drugs
Nitrazepam, Zopiclone
Mechanism of action
Nitrazepam and Zopiclone bind to the GABA-receptors (not in the active site of receptors, but in additional (allosteric) site of receptors) and potentiate GABAergic inhibition of central nervous system.
NB! GABA-receptors = receptors for gamma-aminobutyric acid
Pharmacological effects
These drugs induce the inhibition of central nervous system below normal state and produce the sleeping.
Indications
Insomnia
Nitrazepam, Zopiclone → potentiation of GABAergic inhibition of central nervous system → producing of sleeping.
Antiepileptic drugs (anticonvulsants)
List of drugs
Carbamazepine, Ethosuximide, Diazepam
Mechanism of action
You should study only the mechanism of action of Diazepam. Diazepam binds to the GABA-receptors (not in the active site of receptors, but in additional (allosteric) site of receptors) and potentiate GABAergic inhibition of central nervous system.
Pharmacological effects
These drugs decrease excitement state in the focus of epilepsy in the brain.
Indications
Status epilepticus (epileptic seizures are prolonged, or occur in a series) (Diazepam).
Diazepam → potentiation of GABAergic inhibition of central nervous system → decreasing of excitement state in the focus of epilepsy in the brain → relieving of status epilepticus.
SIMPLICIFIED VERSION