Terima kasih atas penugasan ringkasan tentang toksikokinetika, toksisitas, dan metode deteksi ganja, kokain, dan amfetamin. Saya akan mengerjakannya dan mengirimkan hasilnya kemudian.

1. TOXICITY OF THERAPEUTIC
AGENTS

2. TABLE OF CONTENTS
1. Sedative/ Hypnotics
2. Opioids and derivatives
3. Sympathomimetics
4. Hallucinogenic Agents
5. Anticholinergic and Neuroleptic Drugs
6. Acetaminophen, Salicylates, and
Nonsteroidal Anti-inflammatory Drugs
7. Anabolic-Androgenic Steroids
8. Cardiovascular Toxicology
9. Antineoplastic Agents
10. Vitamins
11. Herbal Remedies

4. a. Barbiturate
b. Benzodiazepines
c. Chloral Hydrate
d. Meprobamate (Miltown, Equanil)
e. Zolpidem Tartrate (Ambien)
f. Buspirone (Buspar)
g. Flunitrazepam (Rohypnol)
h. γ-Hydroxybutyrate
i. Ethchlorvynol (Placidyl)
j. Glutethimide (Doriden)
k. Methaqualone (Quaalude)
l. Methyprylon (Noludar)
1. Sedative/ Hypnotics

7. Toxicokinetics and Metabolism
● An increase in the number of carbons and bulkier side chains results in
enhanced lipid solubility with a corresponding increase in toxicity
● Metabolism occurs primarily in liver (oxybarbiturates)
● Thiobarbiturates are also metabolized to a limited extent in the kidney and
brain
● Phase I reactions introduce polar groups at the C5 position of oxybarbiturates,
transforming the radicals to alcohols, ketones, and carboxylic acids.
● These inactive metabolites are eliminated in urine as glucuronide conjugates
● Side chain oxidation at the C5 position is the most important biotransformation
reaction leading to drug detoxification

8. Mechanism of Toxicity
● CNS depression accounts for all of the toxic manifestations of barbiturate
poisoning
● Barbiturates decrease postsynaptic depolarization by acetylcholine, with
ensuing postsynaptic block, resulting in smooth, skeletal, and cardiac muscle
depression
● At higher doses, barbiturates depress medullary respiratory centers, resulting in
inhibition of all three respiratory drives (neurogenic drive, chemical drive, and
hypoxic drive)

9. Method of Detection
● Gas Chromatography

10. 1) Opioid (Morphine)
2) Codein
3) Diphenoxylate
4) Fentanyl
5) Meperidine
6) Pentazocine
7) Propoxyphene
8) Hydrocodone/Oxycodone
9) Tramadol
10) Clonidine
2. Opioids and derivatives

11. Toxicokinetics and Metabolism
● Rapidly absorbed from an oral dose and from intramuscular (IM) and
subcutaneous (SC) injections
● Peak plasma levels occur at 14 to 60 minutes
● Morphine is metabolized extensively, with only 2% to 14% excreted as the
parent molecule, while 60% to 80% is excreted in the urine as the conjugated
glucuronide
● Heroin is rapidly biotransformed first to monoacetylmorphine and then to
morphine
● Morphine levels rise slowly, persist longer, and decline slowly
● Codeine is extensively metabolized, primarily to the 6-glucuronide conjugate
● Codeine, norcodeine, and morphine in freeand conjugated forms appear in the
urine after codeine ingestion

12. Toxicity and Symptoms
● Attacking central nervous system (CNS)
● CNS depression, respiratory depression, respiratory arrest
● Fifty percent of acute opioid overdose is accompanied by a frothy and
pulmonary edema
● Loss of consciousness and hypo-ventilation
● Bradycardia, hypotension, anddecreased GI motility

13. Method of Detection
● Enzyme-linked Immunoassay (EMIT, KIMS)
● Radioimmunoassay (RIA)
● GC and GC-MS for confirmation methods

14.  Drugs that mimic the stimulation of the sympathetic nervous system
1) Amphetamine
2) Cocaine
3) Xanthine derivatives (caffeine, theophylline, theobromine)
4) Strychnine
5) Nicotine
6) Ephedrine
7) Phenylpropranolamine
8) Pseudoephedrine
3. Sympathomimetics

15. 1) Ergot alkaloids
2) Lysergic acid diethylamide (LSD)
3) Tryptamine derivatives
4) Phenethylamine derivatives (mescaline, 2,5-dimethoxy-4-methylamphetamine (DOM),
3,4-methylene-dioxyamphetamine (MDA)/ ectassy)
5) Phencyclidine
6) Marijuana
7) Other hallucinogenic agents (ketamine, γ-Hydroxybutyrate)
4. Hallucinogenic Agents

16. 1) Antihistamines, gastrointestinal and anti-parkinson drugs
2) Tricyclic antidepressants
3) Phenothiazine, phenylbutylpiperidine, and thioxanthine antipsychotics
4) Selective serotonin reuptake inhibitors (for the management of manifestations of
psychiatric disorders, including the management of clinical depression, obsessive
compulsive disorder (OCD), major depressive disorder (MDD), bipolar disorder, panic
disorders, and syndromes that affect mood and behavior)
5. Anticholinergic and Neuroleptic Drugs

17. 1) Acetaminophen
2) Salicylates and acetylsalicylic acid
3) Nonsteroidal anti-inflammatory drugs (NSAIDs)
6. Acetaminophen, Salicylates, and Nonsteroidal
Anti-inflammatory Drugs

18. 1) Neuroendocrine drugs
2) Anabolic-androgenic steroids
3) Estrogen and progestins
7. Anabolic-Androgenic Steroids

19. 1) Digitalis glycosides
2) β-adrenergic receptor antagonists
3) Calcium channel antagonists (Ca2+ channel blockers)
4) Other cardiovascular drugs
a. ACE inhibitors (captopril, benazepril, enalapril, ramipril, etc)
b. Direct vasodilators (hidralazine, minoxidil, diazoxide, nitroprusside)
c. Antiarrhythmic drug
8. Cardiovascular Toxicology

20.  traditionally referred to as chemotherapeutic agents, are used therapeutically in the
treatment of cancer
1) Antimetabolites
2) Alkylating agents
3) Chemotherapeutic drugs
9. Antineoplastic Agents

21. 1) Fat-soluble vitamins (A, D, E, K)
2) Water-soluble vitamins (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine,
cyanocobalamin, folic acid, Ascorbic Acid)
10. Vitamins

22. 11. Herbal Remedies

23. CREDITS: This presentation template was created by
Slidesgo, including icons by Flaticon, infographics & images
by Freepik and illustrations by Stories
THANKS

24. Reference
 Frank A. Barile. Clinical Toxicology: Principles and Mechanisms
(Chapter 13 – 23)

25. TUGAS RUMAH
Buatlah ringkasan poin tentang
a. Toksikokinetika
b. Toksisitas
c. Metode deteksi
dari bahan terapi Ganja, Kokain, dan Amfetamin