Call Girls Hsr Layout Just Call 7001305949 Top Class Call Girl Service Available
Substance abuse1
1.
2. Substance Abuse
Substance abuse
– Use of drug interferes with ability to function
Fails to meet work or family obligations
– No physiological dependence
Substance dependence (addiction)
– Involves either tolerance or withdrawal
– Tolerance
Greater and greater amounts of substance are needed to produce
the desired effect
– Withdrawal
Physiological and psychological consequences when individual
discontinues or reduces substance use
– Restlessness, anxiety, cramps, death
3. Alcohol-Related Disorders
Discontinuation of alcohol in heavy user:
– Anxiety
– Depression
– Weakness
– Restlessness
– Difficulty sleeping
– Muscle tremors
• Face, fingers, eyelids, other small musculature
– Elevated BP, pulse, temperature
4. Management of Alcohol
Withdrawal
General Measures
Seizure precautions with h/o Sz
Hydration
Thiamine 100mg IM/IV prior to glucose
Correct electrolytes—Mg, Ca, K, PO4
Treat concurrent illnesses
5. Management of AWS
Benzodiazepines (BDZ)
Treatment of choice
Reduce symptoms and decrease risk of Seizurezs
Phenobarbital
Narrow therapeutic index
Carbamazepine
Effective alternative, less sedation
Mayo-Smith JAMA 1997;278:144-51
6. Choice of Benzodiazepine
All seem effective for AWS
Limited comparative data
All metabolized by liver
Differences
Onset of action, half life, routes
1 or 2 step metabolism; active metabolites
Long vs shorter acting
7. Long-acting Benzodiazepines
Chlordiazepoxide (Librium®)
Oral dosing only
Intermediate onset
Long-acting parent compound and metabolites
Smoother withdrawal, less sz, better cognitive fxn
Potential accumulation in elderly and patients with liver
disease
[Diazepam]
8. Shorter-acting BDZs
Lorazepam (Ativan®)
Versatile dosing—PO, IV, IM, SL
Fast to intermediate onset
Intermediate half-life, no metabolites
Less likely to accumulate in elderly or with liver
disease
Breakthrough sx, met. acidosis, delirium
[Oxazepam]
10. Benzodiazepines
Route of administration
Oral preferable
Ease of administration
More consistent blood levels
Sublingual if NPO
(e.g., surgical patients)
Intravenous
Severe w/d requiring rapid titration or NPO
11. Amphetamine Related
Disorder
DSM IV
Amphetamine induced
Anxiety disorder
Mood disorder
Psychotic disorder with delusions
Psychotic disorder with hallucinations
Sexual dysfunction
12. Amphetamine Related
Disorder
Treatment
None established
Treat specific symptoms
Comorbid conditions such as depression may
respond to antidepressants
Bupropion (Wellbutrin)
Used after patients withdraw from amphetamines
13. Caffeine-Related Disorder
Caffeine is an methylxantine
More potent than other known methylxantines
Theophyline (Primatene)
Half-life- 3-10 hrs
Peak 30-60 minutes
Crosses BBB
Adenosine-receptor antagonist
14. Amount of Caffeine
Consumption
Beverages / Food:
Cup of coffee: 65-120 mg caffeine
Espresso 1oz shot: 40 mg
Cup of tea: 40-60 mg
Can of soda: 30-60 mg
Red Bull (8.3oz): 80 mg
Hershey’s milk chocolate almond bar (6oz): 25mg
Over the counter medicines:
No-Doze: 100 – 200 mg
Midol: 20-100 mg
Excedrin: 30-65 mg
Benowitz, 1990
Total consumption of caffeine per person per day is estimated at
210 to 238 mg (Barone and Roberts, 1996)
15. Mechanism of Action
Three main hypotheses:
1. Mobilization of intracellular calcium
Biphasic effect on intracellular calcium levels
*Toxic amounts of caffeine
2. Inhibition of phosphodiesterase
Inhibition of enzyme that breaks down cyclic adenosine monophosphate
(cAMP)
*Toxic amounts of caffeine
3. Antagonism of inhibitory presynaptic adenosine receptors
Caffeine blocks adenosine receptors
Resulting in the inhibition of the breakdown of cAMP
Blocking the inhibitory effects of adenosine
Nehlig et al., 1992
16. Pharmacodynamics
Caffeine
Central Nervous System Enhances neurotransmitter release
Stimulates locomotor activity
Decreases cerebral blood flow
Cardiovascular Release of epinephrine (adrenaline) which
Increases heart rate
Increases blood pressure
Increases blood flow to the muscles
Decreases blood flow to skin and inner
organs
Renal Diuresis; stimulates renal release
Vasculature Peripheral: Dilation
Central: Constriction
Gastrointestinal Increases gastric secretions
Respiratory Bronchodilation
Increases respiratory rate
Garrett and Griffiths 1997
17. Pharmacokinetics
Absorption
Gastrointestinal tract and stomach
Rapid rate, peak blood level in 30-60 min.
Crosses lipid-membrane (not water soluble)
Distribution
Diffuses throughout the organism and crosses BBB
Including placenta and placental BBB
Nehlig et al., 1999; Fredholm et al., 1999
18. Pharmacokinetics
Metabolism
Metabolized through liver biotransformation initially by demethylation into
dimethylxanthines.
*Dimethylxanthines are pharmacologically active and may add to the
effects of caffeine consumption in humans.
This process is unique to humans, no other animal species metabolizes
caffeine in a similar way
Half life of caffeine
Three to eight hours; varies with age and other external factors
Newborns cannot metabolize caffeine, mainly eliminated by excretion
Half life 80 +/_ 23 hours
Smokers, half life is reduced up to 50%
Pregnant women and those taking oral contraceptive, half life up to 15
hours longer
Nehlig et al., 1999; Fredholm et al., 1999
19. Treatment of Caffeine-Related
Disorders
Reducing or eliminating caffeine
consumption
ASA
Headaches, muscle aches from withdrawal
Benzodiazepines-rarely required
20. Cannabis-Related Disorders
Major active ingredient Physiological
– THC (delta-9- – Bloodshot & itchy eyes
tetrahydrocannabinol) – Dry mouth and throat
• Psychological – Increased appetite
– Feelings of relaxation and – Reduced pressure within the
sociability eye
– Rapid shifts of emotion – Reduced BP
– Interferes with attention, – Abnormal heart rate
memory, and thinking • May exacerbate preexisting
– Heavy doses can induce cardiovascular problems
hallucinations and panic – Damage to lung structure and
– Impairment of skills needed function
for driving – Tolerance may develop
• Impairment present for
several hours after ‘high’ has
worn off
21. Cannabis Withdrawal
No specific treatment
Abstinence and support
Anxiolytics
Short-term withdrawal symptoms relief
If depressive disorder is present, treat with
antidepressants
22. Cocaine-Related Disorder
Alkaloid obtained from coca Overdose
leaves – Chills, nausea, insomnia,
– Reduces pain paranoia, hallucinations, and
– Produces euphoria other psychotic symptoms
– Heightens sexual desire – Can cause heart attack and
– Increases self-confidence and death because drug causes
indefatigability blood vessels to narrow
Blocks reuptake of dopamine in • Not all users develop tolerance
mesolimbic areas of brain – Some become more sensitive
• May increase risk of OD
• Usage increased in 70s and 80s
– Dropped late 80s; rose mid 90s
In 2003, 2.3 million users over
the age of 12 (SAMHSA, 2004)
23. Cocaine-Related Disorder
Crack
– Form of cocaine that become popular in the
80s
– Rock crystal that is heated, melted, & smoked
– Increased popularity because it is cheaper than
cocaine
24. Cocaine-Related Disorder
Treatment
No pharmacological treatments produce decreases in
cocaine use comparable to the decreases in opioid use
when heroin users are treated with methadone,
levomethadyl and buprenorphine.
Methylphenidate (Ritalin),Lithium (Eskalith)
Cocaine users presumed to have preexisting ADHD and
mood disorders
Those drugs are useless in patients without the
disorders
25. Cocaine-Related Disorder
Treatment, cont.
Many different treatments have been use with
little or no effects
TCAs
MAOIs
SSRIs
Antipsychotics
Etc.
26. Hallucinogen-Related Disorders
Natural and synthetic substances
Psychedelics or psychomimetics
Induce hallucinations or disconnection with reality
Schedule 1 drugs
28. Hallucinogen-Related Disorders
LSD
Synthesized in 1938
Classic synthetic hallucinogen
MDMA- erroneously classified as a hallucinogen,
vstructirally related to amphetamines
29. Hallucinogen-Related Disorders
Treatment
Symptom specific
Psychological support
Hallucinogen intoxication can be treated with
diazepam 20 mg
Stops LSD effect and associated panic to a stop
within 20 minutes
33. Inhalants-Related Disorders
Intoxication requires no medical attention
Effects of intoxication may require attention
Coma, bronchospasm, laryngospasm, cardiac
arrhythmias, or burns
Sedation is contraindicated
Confusion, panic or psychosis
Severe agitation
Haloperidol 5mg IM/70 kg bw
34. Nicotine-Related Disorders
One of the most highly addictive drugs in the
US.
Known to cause conditions such as:
Cancer, emphysema and CV disease
Secondhand smoke is associated with lung cancer
in adults and respiratory disease in children
35. Nicotine-Related Disorders
According to the DSM IV TR, there is a diagnosis of
nicotine dependence and withdrawal but not of nicotine
abuse or intoxication.
Nicotine dependence occurs very quickly due to
activation of the ventral tegmental area dopaminergic
system.
It is enhance by social factors that encourage or promote
smoking
36. Nicotine-Related Disorders
Pharmacotherapy
Nicotine replacement therapies
Considered to double cessation rates
Can also be used to reduce withdrawal rates in patients
Maintenance period of 6-12 weeks followed by a gradual
withdrawal of another 6 to 12 weeks
Nicotine palicrex gum (Nicorette)
Releases nicotine via chewing and buccal absorption
2 mg for patients who smoke less than 25 cigarretes a day
4 mg for patients that smoke more than 25 cigarretes a day
37. Nicotine-Related Disorders
Pharmacotherapy Varenicline (Chantix)
Non-nicotine medications Chantix is supplied in doses of 0.5 mg
(white) and 1 mg (blue) tablets
Bupropion (wellbutrin) – You may start with an initial Chantix dose
of 0.5 mg once a day
150 mg/day for 3 days
You may increase the Chantix dose to 0.5
Increase to 150 mg twice a mg twice daily after 3 days
day for 6 to 12 weeks Chantix dosage is increased to 1 mg twice
300 mg/day doubles the daily after 7 days
Chantix is generally taken with a glass of
quit rate in smokers with or water after food
without depression Don't skip doses and double dose for
Clonidine (Catapress) missed Chantix dose
decreases sympathetic
activity
Patch or orally 0.2 to 0.4
mg/day may cause
drowsiness
39. Phencyclidine-Related Diorders
Treatment
NO DRUG KNOWN TO FUNCTION AS A DIRECT PCP
ANTAGONIST
Treatment of PCP intoxication aims at reducing
systemic levels of PCP
Address significant, medical, behavioral and
psychiatric issues
40. Sedative, Hypnotic or Anxyolitic-
Related Disorders
Sedatives and Anxiolytics
Drugs that reduce subjective tension and induce
mental calmness
Hypnotics
Drugs that induce sleep
In low dosages instead of inducing sleep, produce
daytime sedation as do sedatives and anxiolytics
Benzodiazepines, Barbiturates, barbiturate-like
substances
41. Sedative, Hypnotic or Anxyolitic-
Related Disorders
Withdrawal Treatment
Carbamazepine
Useful in the treatment of benzodiazepine withdrawal
Refer to table 12.12-6 Guidelines for treatment of
Benzodiazepine withdrawal
Barbiturate
Caution with sudden withdrawal to prevent sudden
death. See table 12.12-7 pg 459
42. Anabolic-Androgenic Steroid Abuse
Family of drugs composed the natural male
hormone Testosterone
Psychiatric concerns
AAS Withdrawal
AS-induced mood disorders
AS-induced Psychotic Disorder
AS-related disorder not otherwise specified
43. Anabolic-Androgenic Steroid Abuse
Treatment
Abstinence
Withdrawal
Supportive therapy and monitoring
Hospitalization may be required if patient presents
suicidal ideation
SSRIs recommended only in patients that present
depressive symptoms weeks after discontinuation of
AAS use
NSAIDs- may be useful in treating muscle aches and
headaches caused by withdrawal.