Presentation is loading. Please wait.

Presentation is loading. Please wait.

Stimulant Drugs Part 1 Kim Edward Light, Ph.D. Professor, College of Pharmacy University of Arkansas for Medical Sciences.

Similar presentations

Presentation on theme: "Stimulant Drugs Part 1 Kim Edward Light, Ph.D. Professor, College of Pharmacy University of Arkansas for Medical Sciences."— Presentation transcript:


2 Stimulant Drugs Part 1 Kim Edward Light, Ph.D. Professor, College of Pharmacy University of Arkansas for Medical Sciences

3 Stimulant Drugs Objectives 1. Identify specific drugs that act as stimulants 2. Outline the general physiological alterations produced by stimulants 3. Identify common therapeutic uses 4. Identify different pharmacological mechanisms of stimulant drug action 5. Discuss the negative consequences of stimulant drug use 6. Discuss the pharmacology of the most common stimulant drugs including their actions, mechanisms, common doses, kinetics, and consequences from acute and chronic use.

4 Drugs ALTER physiological actions rather than create unique effects. A simple means of classifying drugs of abuse can be devised based on the general nature of the drug’s actions. The function of the brain,  Thinking,  Feeling,  Behavior. Classifying Drugs of Abuse

5 Three categories Stim-ul-ants ® – increase thinking, feeling, and behavior Classifying Drugs of Abuse Depress-ants® – decrease thinking, feeling, and behavior Confuse-ants® – distort or confuse thinking, feeling, and behavior ® University of Arkansas

6 Overall Actions Increase  central nervous system arousal and activity.  cardiovascular activity. Neurotransmitters involving adrenergic amines (norepinephrine, epinephrine, dopamine), cholinergic, adenosine, and/or serotonin.

7 Stimulant Drugs Nicotine Caffeine Ephedrine, pseudoephedrine, and related Amphetamine, Methamphetamine Methylphenidate, phenmetrazine, and others Cocaine Psychostimulant plants – Khat, Betel

8 Physiological Actions ↑ activity, alertness, sensory awareness, and reflexive responding (e.g. startle reflex). ↑ cardiovascular activity (HR, BP) Shift blood flow from skin and mesenteric systems to the skeletal muscles (fight or flight). ↑ renal blood flow and diuresis. ↑ in the rate and depth of respiration. ↑ Bronchial dilation. ↓ appetite – by activating satiety.

9 Therapeutic Uses Sleep disorders - narcolepsy, hypersomnia, excessive daytime sleepiness. Attention disorders – ADD or ADHD Weight loss Nicotine dependance Nasal congestion and stuffiness Bronchial asthma and related difficulties Vasoconstriction with local anesthesia

10 Acute Effects Alert and sense of well-being Irritable, aggressive, hyperthermic, hypersexual, nervous, anxious Seizure, stroke Hypertension, cardiac palpitations, arrhythmia, heart attack

11 Chronic Effects Insomnia, paranoia, fearfulness Nervousness, aggressiveness, irrational Nutritional deficits, weight loss, dehydration

12 History Tobacco / Nicotine Columbus credited with introducing plant to Europe. Jean Nicot, the French ambassador to Portugal, provided its name Nicotiana tabacum. Nicotine was isolated in 1828.

13 Tobacco / Nicotine Facts The primary source of nicotine is tobacco. Tobacco is  smoked  chewed  snuffed

14 Nicotine Mechanism of Action Acts on a subtype receptors for acetylcholine.  Brain  Autonomic ganglia  Adrenal medulla

15 Nicotinic Effects Adrenal medulla – ↑HR ↑ BP Brain - Reward Pathway Other brain functions  pain relief - analgesia  memory  cognition - thinking  learning.

16 Therapeutic Uses Present  Patch, gum, lozenge, or inhaler form to discontinue smoking Future  Treatment of chronic pain, Alzheimer's disease, schizophrenia

17 Toxic Effects of Nicotine Carcinogenic (cancer causing) Diminished respiratory and cardiovascular function Depression of the immune system. Remember – Nicotine is responsible for the use of tobacco!!

18 Nicotine / Pharmacokinetics Absorbed - rapidly Distributed throughout the body Metabolized in the liver - produces cotinine as one metabolite. T 1/2 of approximately two hours, Excreted in the milk of nursing mothers who smoke.

19 History of Caffeine Oldest drug used by humans Stories of discovery:  Zen Buddhist  Chinese emperor  Kaldi, the Arabian goat herder

20 Making Coffee Coffea arabica Made from seeds of Coffea arabica Seeds encased in berries (or cherries). Fruit pulp is fermented to free the seeds. Roasting and grinding bring out essential oils for flavor and allow the extraction of caffeine

21 Coffee History 1615 – introduced to Europe 1700 coffee houses popular in Europe. Late 1700s Dutch East Indies plantations Early 1800s Plantations Caribbean & South America Today Brazil and Columbia are world’s leading producers.

22 Making Tea Camellia Sinensis From leaves of Camellia sinensis. The leaves are plucked, dried and ground to allow oxidation of the constituents thus increasing flavor.

23 History of Tea The Portuguese Jesuit Father Jasper de Cruz on a missionary trip to China around 1560. Along with the Dutch, the Portuguese developed the tea trade. Introduced to England between 1652 and 1654.

24 Caffeine Content Common Products Drip coffee.....115 mg Tea..................40 mg Cocoa..............13 mg Coca Cola........46 mg Diet Coke.........46 mg Dr. Pepper........40 mg Mr. Pibb............41 mg Mt. Dew............54 mg Pepsi...............38 mg Surge...............51 mg Jolt Cola...........71 mg Excedrin...........65 mg Anacin..............32 mg NoDoz............100 mg Vivarin............200 mg Midol...............600 mg

25 Caffeine Acts on the central and peripheral nervous systems Member of a group of drugs called methylxanthines

26 Actions of Methylxanthines Caffeine - most active as a CNS stimulant. Theophylline - most active outside the CNS. Theobromine - least active  Differences are related primarily by potency and site of action. Act as antagonists of adenosine receptors.  Adenosine is the neurotransmitter/neuromodulator

27 Actions of Caffeine CNS stimulation - alertness and wakefulness, Increased capacity for sustained intellectual effort and clear thinking Increase in Heart Rate and force Smooth muscle relaxation especially in respiratory track. Diuresis (increased urine production)

28 Pharmacokinetics Absorption is nearly 100% Peak levels at 15-120 minutes. T 1/2 of 3-5 hours. Distribution is seen in all sites in the body Metabolized by the liver Excreted in the urine - less than 5% of excreted as the parent compound

29 Caffeine Typical doses from 40 – 150 mg. With short duration, doses are repeated every 2-4 hours (“coffee breaks”) Doses >200-250 mg likely to produce extreme agitation.

30 Caffeine - High Doses Extreme nervousness, insomnia, restlessness, and tremors Convulsions Rapid heart rate Increase contractile force of the heart Cardiac arrhythmias Increased blood pressure Diuresis

31 Long Term Consequences Nervousness, Irritability, Insomnia Increased heart rate, hypertension Gastric distress and ulcers Increased serum cholesterol

32 Athletics and Caffeine No significant effect on athletic performance The NCAA limit for caffeine in urine is 15 micrograms per ml.  Example: 2 cups coffee = urine levels of 3-6 micrograms per ml.

33 Caffeine Abuse Dependance and withdrawal Caffeine addiction = “caffeinism” Caffeine in very high doses available in “look-alike” pills - “legal stimulants” Dietary supplement products for increased energy or appetite suppression.

34 Summary General aspects of stimulant drugs. Common physiological actions. Overview of therapeutic usefulness. Adverse effects - acute and chronic. Differing mechanisms of action. Nicotine from tobacco. Caffeine from coffee, tea, other sources.

Download ppt "Stimulant Drugs Part 1 Kim Edward Light, Ph.D. Professor, College of Pharmacy University of Arkansas for Medical Sciences."

Similar presentations

Ads by Google