MT6314 SUBSTANCE OF ABUSE Flashcards
1
Q
The primary kind of alcohol which is a substance of abuse is?
A
ethyl
2
Q
Occupies an important place in history of mankind
A
Alcohol
3
Q
Main alcohol staple of western countries in the 19th century?
A
Beer and wine
4
Q
Alcohol is known to be associated with?
A
acute and chronic
illnesses
5
Q
Moderate amount of alcohol relieves and provides what?
A
relieves anxiety and provides feeling of euphoria
6
Q
The most commonly abused drug in the world
A
Alcohol
7
Q
continue consumption despite
suffering consequences
A
Alcohol abuse
8
Q
inability to control drinking, devoting much time to getting and using alcohol, or recovering from its effects
A
Alcohol dependence
9
Q
use disorders are complex; has genetic and environmental factors
A
Alcohol
10
Q
Is ethanol water soluble?
A
Yes
11
Q
Where does ethanol absorb rapidly in the body?
A
gastrointestinal tract
12
Q
In fasting state, peak blood alcohol concentrations are reached within how long?
A
30mins
13
Q
What delays alcohol absorption by slowing gastric emptying?
A
Food
14
Q
Alcohol distribution: rapid or slow?
A
Rapid
15
Q
Volume of distribution for ethanol approximates?
A
total body water (0.5–0.7 L/kg)
16
Q
T or F: Women have a higher peak concentration than men
A
T
17
Q
Why do women have a higher peak concentration than men?
A
Women have a lower total body water content and differences in first-pass metabolism
18
Q
In CNS, concentration of ethanol rises (slowly/quickly)
A
Quickly
19
Q
Why in the CNS, concentration of ethanol rises quickly?
A
Brain receives a large proportion of total blood flow and ethanol readily crosses biologic membranes
20
Q
> 90% of alcohol is oxidized in? And the remainder in where?
A
the liver
remainder excreted through the lungs and in the urine
21
Q
Excretion by the lungs can be quantified with?
A
breath alcohol tests
22
Q
Alcohol Oxidation follows what order of kinetics?
A
zero-order kinetics
23
Q
Typical adult can metabolize how many grams of alcohol per hour?
A
7–10 g (150–220 mmol)
24
Q
Primary pathway for alcohol metabolism
A
Alcohol Dehydrogenase Pathway
25
Where is Alcohol Dehydrogenase Pathway mainly located?
Liver (main), brain, stomach
26
What about the alcohol dehydrogenase pathway affects the rate of ethanol metabolism and alters vulnerability to alcohol-abuse
disorders?
considerable genetic variation in ADH enzymes
27
Is metabolism by ADH greater in men or women? and why?
Men bec. of sex-related differences in
blood alcohol concentrations
28
The Microsomal Ethanol-Oxidizing System (MEOS) uses ____ and consists of _____
uses NADPH, consists
primarily of cytochrome P450 enzyme group
29
When is MEOS activity induced?
during chronic alcohol
consumption, also when blood levels are >100mg/dL
30
What happens in chronic alcohol consumption?
significant increases in ethanol metabolism and the clearance of other drugs eliminated by the cytochrome P450s that constitute the MEOS system
31
Much of the acetaldehyde formed is oxidized in the liver in a reaction is catalyzed by?
Aldehyde dehydrogenase (ALDH)
32
What is the product of Acetaldehyde Metabolism?
acetate
33
used to deter drinking by patients with alcohol dependence
Disulfiram
34
Acetaldehyde accumulates and causes an unpleasant reaction of facial flushing, nausea, vomiting, dizziness, and headache
Disulfiram + Ethanol
35
Examples of drugs that inhibit ALDH? What od these drugs do?
metronidazole, cefotetan, trimethoprim
Cause a disulfiram-like reaction if combined with ethanol
36
People of what descent have a genetic deficiency of ALDH?
East Asian descent
37
What happens to East Asians since they have deficiency in ALDH?
Consuming alcohol, they develop high blood acetaldehyde concentrations and experience a reaction similar to that seen with the combination of disulfiram and ethanol
Asian flush
38
What effect does alcohol have on the CNS?
sedation, relief of anxiety
39
At higher concentrations of alcohol, what does it cause to the CNS?
ataxia, impaired judgment, and
disinhibited behavior
40
Additive CNS depression occurs with concomitant ingestion of?
Ethanol and a variety of CNS depressants such as sedative-hypnotics, opioid agonists, and drugs that block muscarinic and H1 histamine receptors.
41
Ethanol appears to modulate the function of?
Signaling molecules such as the action of GABA at GABAA receptors, inhibits the ability of glutamate to activate NMDA receptors and modifying the activities of adenylyl cyclase, phospholipase C, and ion channels
42
What BAC levels leads to sedation and depression of myocardial contractility?
50-100: sedation
>100: depression of myocardial contractility
43
What BAC levels leads to emesis and stupor?
200-300
44
What BAC levels leads to coma?
300-400
45
What BAC levels leads to respiratory depression and death?
>400
46
What BAC levels leads to impaired motor function, slurred speech, ataxia?
100-200
47
Ethanol, in relation to smooth muscles, is also a?
vasodilator
48
In severe alcohol overdose, what happens to the Smooth muscles?
hypothermia Bec. of vasodilation
49
What augments the hypotensive effects of ethanol,
may cause severe orthostatic hypotension and syncope?
Flibanserin
50
T or F: Ethanol also vasodilator the uterus
F, it relaxes it
51
How does alcohol cause tissue damage?
Oxidative stress with depletion of glutathione, damage to mitochondria, growth factor
deregulation, potentiation of cytokine-induced injury
52
What kind of tolerance facilitates GABA activity?
Cross-tolerance to sedative-hypnotic drugs
53
What kind of dependence is seen in chronic alcohol consumption?
Psychological and physical
54
Most common medical complication that comes with chronic alcohol consumption?
Liver disease
55
Reduced gluconeogenesis leads to?
Hypoglycemia
56
Progressive loss of liver function, with reversible fatty liver leads to?
irreversible hepatitis, cirrhosis, and liver failure
57
In both sexes infected with hepatitis B or C, is hepatic dysfunction more severe in men or women?
Women
58
Consequences of chronic alcohol consumption on the GI tract?
Irritation, inflammation, bleeding, and scarring of the gut wall
absorption defects and exacerbation of nutritional
deficiencies
increases the risk of pancreatitis
59
Consequences of chronic alcohol consumption on the CNS?
Peripheral neuropathy
Wernicke- Korsakoff
syndrome
60
What causes Wernicke- Korsakoff syndrome? and what is it characterized by?
Thiamine deficiency, along with alcohol abuse
characterized by ataxia, confusion, and paralysis of the
extraocular muscles
61
How to treat Wernicke- Korsakoff syndrome? This treatment is essential to prevent?
Treatment with parenteral thiamine is essential to prevent Korsakoff’s psychosis: a permanent memory disorder
62
Alcohol withdrawal symptoms with forced quitting/reduction causes?
hyperexcitability in mild cases; seizures, toxic psychosis, and delirium tremens in severe ones
63
Effects of chronic alcohol consumption to the endocrine system and electrolyte balance?
Gynecomastia and testicular atrophy
Ascites, edema, and effusions
Alterations of whole body potassium
Severe secondary aldosteronism
Hypoglycemia
64
Effects of chronic alcohol consumption to the cardiovascular system?
Hypertension, anemia, and dilated
cardiomyopathy
Binge drinking = arrhythmia
Modest quantities = HDL goes up
65
Effects of chronic alcohol consumption to the immune system?
Some immune functions inhibited, some triggered
Lungs: suppressed alveolar macrophage function, inhibition of chemotaxis of
granulocytes, reduced T cells, increases mortality & morbidity of pneumonia
Liver: enhanced function of cells in immune system, increased cytokine production
66
Chronic alcohol use also leads to increased risk of what cancers?
Cancer of the mouth, pharynx, larynx, esophagus, and liver and small increase of breast cancer in women
67
What species produced by increased cytochrome P450
activity can damage DNA?
Acetaldehyde and reactive oxygen
68
What consequence of chronic alcohol consumption has teratogenic effects?
Fetal alcohol syndrome
69
Most commonly stem from alcohol-induced increases of drug-metabolizing enzymes
Prolonged intake without liver damage can enhance the biotransformation of other drugs
ALCOHOL-DRUG INTERACTIONS
70
Ethanol-mediated induction of hepatic cytochrome P450 enzymes is particularly important with regard to?
acetaminophen
(Paracetamol)
71
Chronic or acute alcohol consumption can inhibit metabolism of other drugs - decreased enzyme activity or decreased liver blood flow?
Acute
72
Examples of drugs whose metabolisms are inhibited with acute alcohol use?
Phenothiazines, tricyclic antidepressants, and sedative- hypnotic
drugs
73
Occurs when alcohol is combined with other CNS depressants, particularly sedative-hypnotics
Additive CNS depression
74
What kind of drugs can be used in the management of alcohol withdrawal syndrome?
Long-acting sedative-hypnotic drug replaced for alcohol (Benzodiazepines preferred- chlordiazepoxide, diazepam)
Shorter-acting benzodiazepines- lorazepam and oxazepam
75
Useful in alcoholic patients with liver disease
lorazepam and oxazepam
76
Built in tapering effect where active metabolites may accumulate
Long-acting sedative-hypnotic drug replaced for alcohol
77
Main DRUG TREATMENTS OF ALCOHOLISM
Naltrexone
Acamprosate
Disulfiram
78
Nicotine & Caffeine effects (common)
cardiovascular, respiratory, and neoplastic disease with smoking
addiction and dependence
79
Causes respiratory paralysis
Nicotine
80
Seen in small children who ingest nicotine gum, nicotine patches or vaping solutions
Severe nicotine toxicity
81
Characterized by excessive CNS stimulation with tremor, insomnia, and nervousness; cardiac stimulation and arrhythmias
Acute toxicity for both nicotine and caffeine
82
Nicotine is the selective agonist of?
nicotinic acetylcholine receptor
83
Nicotine is slowly or quickly absorbed?
Slowly
84
Partial agonist action at α4β2 nicotinic receptors
Varenicline
85
Effects of varenicline?
may impair the capacity to drive, associated with suicidal ideation
86
antidepressant is approved for nicotine cessation therapy
Bupropion
87
When is Bupropion most effective?
when combined with behavioral therapies
88
agonist at cannabinoid receptors, used off-label in smoking cessation
Rimonabant
89
Caffeine is a member of what family?
methylxanthine
90
Effects of caffeine on the heart?
Has positive chronotropic and inotropic effects on the heart
91
Antidote to caffeine withdrawal?
Esmolol a short-acting β blocker
92
Inhibits caffeine metabolism
Quinolone
93
What treatment of alcoholism: long acting opioid antagonist, blocks u-opioid receptors
Naltrexone
94
What treatment of alcoholism: Can cause dose-dependent hepatotoxicity, used with caution if with abnormal serum aminotransferase activity
Naltrexone
95
T or F: Naltrexone is usually taken with disulfiram
F, if taken together, will result in hepatotoxicity
96
What treatment for alcoholism: Has actions on GABA, glutamate, serotonergic, noradrenergic, and dopaminergic receptors
Acamprosate
97
What treatment for alcoholism: A weak NMDA-receptor antagonist and a GABAA-receptor activator.
Acamprosate
98
What treatment for alcoholism: Should not be given to patients with severe renal impairment
Acamprosate
99
What treatment for alcoholism: Inhibits aldehyde dehydrogenase, acetaldehyde accumulates
Disulfiram
100
Disulfiram inhibits the metabolism of?
Phenytoin
Oral anticoagulants
Isoniazid
101
What type of alcohol: Used in industrial production of synthetic organic compounds and as a constituent of many commercial solvents, also in windshield-washing products
Methanol/methyl alcohol/wood alcohol
102
Methanol/methyl alcohol/wood alcohol is oxidized to?
formaldehyde, formic acid, and CO2
103
Methanol can also cause poisoning from?
Accidental ingestion
104
Methanol is absorbed well in the?
Skin
Respiratory
GI
105
Treatment for methanol poisoning?
Respiration support
106
Modalities of treatment for severe methanol poisoning?
Suppression of metabolism by alcohol dehydrogenase to toxic products
Hemodialysis
Alkalinization
107
alcohol dehydrogenase inhibitor
Fomepizole
108
higher affinity than methanol for alcohol dehydrogenase saturation reduces formate production
Intravenous ethanol
109
Used as heat exchangers, in antifreeze formulations, and as industrial solvents
Ethylene glycol
110
Stages of overdose of ethylene glycol?
transient excitation followed by CNS depression (first few hours after ingestion)
severe metabolic acidosis (after 4-12 hours)
delayed renal insufficiency
111
Treatment to ethylene glycol overdose?
fomepizole, ethanol, and hemodialysis
112
Alcohol has an additive sedative effect with?
Sedative-hypnotics
113
Alcohol additive vasodilator effect with?
Hypoglycemic agents
114
Alcohol additive anti-platelet action with?
Aspirin
115
Ethylene glycol toxicity is retarded by?
Fomepizole or IV ethanol
116
Alcohol-drug interactions have the induction of?
SER
117
What treatment for alcohol: NMDA antagonist
Acamprosate
118
What treatment for alcohol: Opioid antagonist
Naltrexone
119
What treatment for alcohol: 5-HT3 antagonist
Ondansetron
120
What treatment for alcohol: Aldehyde dehydrogenase antagonist
Disulfiram
121
What treatment for alcohol: Mainly targets CNS NTA system
Naltrexone
