Pharmacology of Drugs

Question 1

Cocaine

Answer 1

Pharmacology: Plant Derivated Weak Base, Cocaine HCl/Cocaine Base, Metabolites are benzolecgonine and cocathylene

Mechanism: Blocks reuptake of DA, NE, 5-HT, and Na+ channels at the axon terminals of its respective pathway

Acute Effect: Increased energy, arousal, concentration, self-esteem, physical performance, weight loss, sympathomimetic effects (fight/flight)

Toxic Effect: Headache, dizziness, confusion, agitation, fatigue, insomnia, nasal bleeding, seizures, cardiac arrest, stimulant psychosis

Therapeutic Uses: Lidocaine for local anesthetic and to reduce blood flow to site

Chronic Use: Constricts coronary artery reducing oxgen reaching heart, exerts direct toxic action on heart, cardiac arryhtmia,

Question 2

Amphetamine

Answer 2

Pharmacology: phenylethylamine, salt and free base form like cocaine, weak base

Mechanism: enhanced released and blocks reuptake of catecholamines, inhibits MAO, agonist at catecholamine receptors (makes signal stronger)

Acute Effects: stimulatory effects

Toxic Effects: bruxism, stimulant psychosis, neurotoxicity, tooth decay, gum disease

Therapeutic Uses: Narcolepsy (most accepted use), ADHD (most common use)

Chronic Uses: Tolerance, dependence

Question 3

Nicotine

Answer 3

Pharmacology: Weak base, nicotrine changes to cotinine via Cytochrome P450,

Mechanism: Nicotonic Ach from the LTD/PPT –> VTA and Nucleus Basilis/Medial Septum –> Cortex/Hippocampus

Acute Effects: Mental stimulation, relaxation, increased respiration, anti-diuresis. After very high doses, dizziness, nausea, respiratory supression, seizures death (>60 mg)

Toxic Effects: Tolerance, dependence, death, carcinogens from tar, reduces oxygen supplement (atherosclerosis, CO reduces affinity of hemoglobin for O2, impairs pulmonary function), COPD (emphysema, bronchitis, asthma)

Therapeutic Uses: Potentially Depression, Schizophrenia, Altzheimer’s disease, Tourette Syndrome, ADHD, nicotine replacement

Chronic Uses:

Question 4

Caffeine

Answer 4

Pharmacology: Xanthine, weak base

Mechanism: Low dose: blockade of adenosis receptors / High doses: inhibition of phosphodiesterase, blockade of GABAa receptors, increased Ca²⁺ relase

Acute Effects: Stimulatory effects, decreased blood flow to brain (increased or decreased headaches), increased respiration rate, increased gastric secretions, diuresis

Toxic Effects: 500-100 mg: anxiety, irritability, insomnia, fever, flushing >1500 mg: paranoia, delusions, hallucinations, stereotypes

Therapeutic Uses: asthma, sleep apnea, narcolepsy, headache (may be helpful for Diabetes Type II, cardiovascular, liver disease, Parkinson’s Disease, antioxidants)

Chronic Uses:Tolerance and dependence (maybe Benign Breast Disease, reproduction, cardiovascular, anxiety disorders, caffeinism, physical dependence)

Question 5

Opiods

Answer 5

Pharmacology: semisynthetic, synthetic, endogenous opiods, weak bases

Mechanism: Inhibits formation of of CAMP via inhibitory Gi protein, postsynaptic inhibition increases K+ efflux, presynaptic inhibition decreases nt release, autoreceptor activation decreases nt release

Acute Effects: sedation, drowsiness, euphoria, pupillary contraction, nausea, vomitting, couching and respiratory suppresion, hypothermia, reduced sexual drive, analgesia, constipation

Toxic Effects: Respiratory failure by medulla, opiod overdose

Therapeutic Uses: Analgesia, anesthesia, cough suppresion, reduce intestinal motility

Chronic Uses: Tolerance (cellular, contextual) and dependence