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Psych Exam II AP > Drugs- Alcohol abuse (linger) > Flashcards

Drugs- Alcohol abuse (linger) Flashcards

1
Q

genes that incur risk to alcoholism?

A

ii) Some candidate genes for susceptibility to alcoholism include the dopamine D4 receptor,

the β1 subunit of the GABAA receptor,

and tyrosine hydroxylase (involved in the synthesis of dopamine, norepinephrine, and epinephrine)

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2
Q

which genes appear to protect against alcoholism

A

i) Some genes appear to protect against alcoholism, such as polymorphisms in alcohol dehydrogenase and aldehyde dehydrogenase

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3
Q

time to peak blood levels of alcohol with empty stomach

A

30 min

ii) Absorption occurs more rapidly from the small intestine than from the stomach
iii) The presence of food delays absorption by slowing gastric emptying
iv) Ethanol undergoes extensive first-pass metabolism by gastric and liver alcohol dehydrogenase (ADH)

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4
Q

metabolism of alcohol?

A

zero order (so independent of time and concentration)

iii) Small amounts of ethanol are excreted in urine, sweat, and breath, but metabolism to acetate accounts for 90-98% of ingested ethanol, mostly owing to hepatic metabolism by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)
(3) Gastric metabolism of ethanol is lower in women than in men, which may contribute to the greater susceptibility of women to alcohol (in addition to a lower total body water content)

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5
Q

how much alcohol per hour can the typical adult metabolize and why ?

A

7-10 g approximately 1 drink

(3) NAD+ requirements for alcohol metabolism
(a) 2 mol of NAD+ are required to convert 1 mol of ethanol to acetic acid (required by both ADH and ALDH)
(b) In terms of weight, 46 g of ethanol requires 1.3 kg of NAD+, which greatly exceeds the supply of NAD+ in the liver and is why the body is only able to metabolize about 7-10 g of alcohol per hour (zero-order metabolism)

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6
Q

alcohol dehydrogenase pathway

A

(2) ADH is a cytosolic enzyme that catalyzes the conversion of ethanol to acetaldehyde and is located predominantly in the liver (others include the stomach and brain)
(4) NAD+ is required to convert ethanol to acetaldehyde (this produces NADH, of which excess production may contribute to the metabolic disorders that accompany chronic alcoholism and to the lactic acidosis and hypoglycemia that frequently accompany acute alcohol poisoning)

(5) Aspirin inhibits gastric ADH and can increase ethanol bioavailability
(6) Fomepizole inhibits ADH and is used in the treatment of acute methanol or ethylene glycol poisoning (see below)

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7
Q

fomepizole

A

(6) Fomepizole inhibits ADH and is used in the treatment of acute methanol or ethylene glycol poisoning (see below)

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8
Q

Disulfiram

A

(4) ALDH is inhibited by disulfiram, a drug used for the treatment of alcohol abuse and dependence (see below)

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9
Q

what is an example of a certain polymorphism of ALDH and what happens in these individuals

A

(5) Genetic polymorphism of ALDH
(a) Some individuals of primarily Asian descent have a low activity level of mitochondrial ALDH
(b) When these individuals drink alcohol, they develop high acetaldehyde concentrations and may experience facial flushing, light headedness, palpitations, nausea, and general “hangover” symptoms
(c) Appears to protect against alcohol dependence and abuse
(d) Individuals with the polymorphism in ALDH who are chronic heavy drinkers and/or alcohol dependent have an increased risk of severe liver disease due to the toxic effects of acetaldehyde

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10
Q

what is the mechanism of action of the microsomal ethanol oxidizing system

A

(1) Mixed function oxidases (cytochrome P450s) use NADPH as a cofactor in the metabolism of ethanol to acetaldehyde
(2) At higher concentrations of ethanol (when NAD+ is depleted and the alcohol dehydrogenase system becomes saturated) there is increased contribution from the P450s, particularly 2E1, 1A2, and 3A4
(3) Chronic alcohol consumption induces MEOS activity (2E1) and can result in the enhanced activation of toxins, free radicals, and hydrogen peroxide

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11
Q

what happens when a person uses disulfiram

A

decrease in alcohol consumption b/c of side effects of nausea, chest pain, hyperventilation, tachycardia, vomiting

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12
Q

intoxication BAC level

A

0.08 %

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13
Q

50-100 BAC

A

Sedation, subjective “high,” slower reaction times

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14
Q

100-200 BAC

A

Impaired motor function, slurred speech, ataxia

at BAC above 100 depression of myocardial contractility has been observed

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15
Q

200-300 BAC

A

Emesis, stupor

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16
Q

300-400 BAC

A

coma

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17
Q

> 500 BAC

A

resp depression, death

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18
Q

effects of alcohol on NMDA

A

glutamate receptor

(a) Glutamate is the primary excitatory neurotransmitter in the CNS
(b) Receptor activation is implicated in many aspects of cognitive function including learning and memory
(c) Alcohol inhibits the ability of glutamate to open the cation channel of the NMDA receptor and leads to an increased depression of the CNS
(d) Memory loss that occurs with high levels of alcohol (i.e., blackouts) most likely results from inhibition of NMDA receptor activation

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19
Q

effects of alcohol on the GABA receptor

A

(a) GABA is the primary inhibitory neurotransmitter in the CNS
(b) Alcohol (like other sedative-hypnotics) enhances the effects of GABA on the GABAA receptor and leads to an increased depression of the CNS

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20
Q

effects of alcohol on smooth muscle

A

i) Ethanol causes vasodilation, likely due to CNS effects (depression of the vasomotor center) and smooth muscle relaxation caused by the metabolite acetaldehyde
ii) In severe overdose situations, ethanol can cause hypothermia caused by vasodilation
iii) Ethanol causes uterine muscle relaxation and was used intravenously for suppression of premature labor before the introduction of more effective and safe medications (e.g., calcium blockers, magnesium ion, β2-adrenergic receptor agonists)

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21
Q

effects of alcohol on the esophagus

A

(1) Alcohol is a factor associated with esophageal dysfunction, esophageal reflux, Barrett’s esophagus, traumatic rupture of the esophagus, Mallory-Weiss tears, and esophageal cancer
(2) At high BAC, decreased peristalsis and decreases lower esophageal sphincter pressure occur (may respond to proton-pump inhibitors and abstinence)

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22
Q

effects of alcohol on the stomach

A

(1) Heavy alcohol use can disrupt the gastric mucosal barrier and cause acute and chronic gastritis
(2) Beverages containing more than 40% alcohol have a direct toxic effect on gastric mucosa with clinical symptoms that include acute epigastric pain (relieved with antacids or histamine H2-receptor blockers

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23
Q

effects of alcohol on the intestines

A

(1) Chronic diarrhea can result in malabsorption of nutrients in the small intestine
(2) Reversible alcohol damage can also result in weight loss and multiple vitamin deficiencies
(a) Deficiencies in B complex of vitamins (particularly thiamine), retinoids and carotenoids
(b) Chronic alcohol consumption has been implicated in osteoporosis
(c) Alcoholics have lowered serum and brain levels of magnesium, which may contribute to a predisposition to brain injuries

24
Q

effects of alcohol on the pancreas

A

(1) Heavy alcohol use is the most common cause of both acute and chronic pancreatitis in the US
(2) Alcohol has direct toxic effects on pancreatic acinar cells, alters pancreatic epithelial permeability, and promotes the formation of protein plugs and calcium carbonate-containing stones

25
Q

what is the most common medical complication of alcohol abuse

A

liver disease

(15-30% of chronic heavy drinkers eventually develop severe liver disease)

(3) Primary effects are progressive: fatty infiltration of the liver (also called alcoholic fatty liver, which is reversible), hepatitis, and cirrhosis leading to liver failure
(4) Accumulation of fat results from inhibition of both the tricarboxylic acid cycle and the oxidation of fat, in part, owing to the generation of excess NADH produced

26
Q

why do seizures occur with withdrawal from alcohol (supposed mechanism)

A

(a) Chronic exposure of animals to alcohol elicits many adaptive responses involving neurotransmitters and their receptors, ion channels, and enzymes that participate in signal transduction pathways
(b) Expression of NMDA receptors and voltage-sensitive Ca2+ channels are up-regulated, which may underlie the seizures that accompany alcohol withdrawal syndrome
(c) GABAA receptors are down-regulated, which leads to a continued hyperexcited state of the CNS during withdrawal

27
Q

symptoms of alcohol withdrawal

A

delirium tremens- delirium, hallucinations, fever, and tachycardia

other symptoms:
HTN
malaise
nausea

28
Q

what is wernicke korsakoff syndrome

A

Caused by vitamin B1 deficiency

Confusion, ophthalmoplegia (paralysis of the external muscles), ataxia

may progress to irreversible memory loss, confabulation, personality change

associated with periventricular hemorrhage/necrosis of mammillary bodies

29
Q

effects of alcohol on the nervous system

A

(1) Degenerative changes of the nervous system occur with chronic alcohol abuse and include the following symptoms:
(a) Generalized symmetric peripheral nerve injury, which begins with distal parathesias of the hands and feet (most common neurologic abnormality of chronic alcoholics)
(b) Gait disturbances and ataxia
(c) Dementia and demyelinating disease (rare)

  1. Wernicke-Korsakoff
    (3) Painless blurring of vision occurs over several weeks of heavy alcohol consumption, with changes typically bilateral and symmetric (optic nerve degeneration may follow)
30
Q

what happens to the cardiovascular system with chronic alcohol consumption

A

(1) Heavy and continued alcohol consumption is associated with a dilated cardiomyopathy with ventricular hypertrophy and fibrosis

arrythmias

HTN

Coronary heart disease
-actually alcohol is PROTECTIVE with moderate consumption (1-3 per day)

Stroke

Anemia (folic acid deficiency, GI bleeds lower iron)

31
Q

what changes occur in heart cells specifically with alcohol consumption chronic

A

(2) Alcohol induces the following changes in heart cells: membrane disruption, depressed function of mitochondria and sarcoplasmic reticulum, intracellular accumulation of phospholipids and fatty acids, and up-regulation of voltage-dependent calcium channels

32
Q

how is alcohol protective for CHD (coronary heart disease)

A

(1) Studies show that moderate alcohol consumption (1-3 drinks per day) prevents CHD and reduces mortality more than in individuals who abstain or are heavy consumers of alcohol (this is now being questioned, however)
(2) Ethanol raises serum levels of the cardioprotective high density lipoprotein (HDL) cholesterol, inhibits some inflammatory processes that underlie atherosclerosis, and antioxidants (especially in red wine) may protect against atherosclerosis

33
Q

Endocrine system changes with alcohol consumption

A

g) Endocrine system and electrolyte balance
i) Possible unbalance of steroid hormones may cause gynecomastia and testicular atrophy
ii) Potassium level alterations, hypoglycemia, and ketosis are possible in heavy drinkers

34
Q

effects of alcohol on the immune system

A

i) Immune function in some tissues is inhibited (lung) while pathologic, hyperactive immune function in other tissues is triggered (liver, pancreas)
ii) Inflammatory damage can occur in the liver while predisposition to infections (e.g., in the lung) can worsen the morbidity and increase the mortality risk of patients with pneumonia

35
Q

effects of alcohol on skeletal system

A

i) Chronic ethanol consumption is associated with decreased muscle strength and increased activity of creatine kinase in the plasma

36
Q

body temp with alcohol consumptoin

A

i) Due to increased cutaneous and gastric blood flow, sweating may occur while the internal body temperature falls

37
Q

alcohol effects of body water volume/ sodium levels with both consumption and withdrawal

A

i) Alcohol inhibits the release of vasopression (antidiuretic hormone; causes reabsorption of water and concentration of urine) from the posterior pituitary gland, resulting in enhanced diuresis
ii) Vasopressin release is increased during withdrawal resulting in water retention and dilutional hyponatremia

38
Q

Fetal alcohol syndrome

A

apoptotic degeneration can happen if consumed during pregnancy

ii) Alcohol is a leading cause of mental retardation and congenital malformation

iii) FAS includes:
(1) Intrauterine growth retardation
(2) Microcephaly
(3) Poor coordination
(4) Underdevelopment of midfacial region
(5) Minor joint abnormalities

iv) Ethanol crosses the placenta and the fetal liver has little or no alcohol dehydrogenase activity and must rely on the mother’s liver for elimination

39
Q

cancer and alcohol?

A

i) Chronic alcohol use increases the risk for cancer of the mouth, pharynx, larynx, esophagus, and liver and may increase the risk of breast cancer in women (though alcohol is not a carcinogen)
ii) Acetaldehyde and reactive oxygen species produced by increased CYP450 activity can damage DNA

40
Q

effects of alcohol on CYP450’s

A

a) Chronic ethanol consumption increases the levels of CYP450s (particularly 2E1)

41
Q

how do you manage acute alcohol intoxication

A

a) Management of acute alcohol intoxication

i) Goals include the prevention of severe respiratory depression and aspiration of vomitus
ii) Glucose can treat metabolic alterations such as hypoglycemia and ketosis
iii) Thiamine is provided to protect against the Wernicke-Korsakoff syndrome
iv) Potassium may be required in the event of severe vomiting (if renal function is normal), along with electrolyte solutions

42
Q

how do you treat alcohol withdrawal

A

ii) Major pharmacological objective is to prevent seizures, delirium, and arrhythmias and include electrolyte rebalancing and thiamine therapy

iii) Drug therapy for detoxification in severe cases involves substituting a long-acting sedative-hypnotic drug for alcohol and then gradually tapering the dose
(1) Long-acting benzodiazepines (chlordiazepoxide, clorazepate, diazepam)
(a) Benefits: less frequent dosing and built-in tapering effect
(b) Disadvantages: pharmacologically active metabolites may accumulate, especially in patients with compromised liver function
(2) Short-acting benzodiazepines (lorazepam, oxazepam)
(a) Rapidly converted to inactive metabolites and are useful in patients with liver disease

43
Q

earliest signs of alcohol withdrawal

Later signs?

A 
anxiety
insomnia
tremor
palpitations
nausea
anorexia

The earliest symptoms (anxiety, insomnia, etc) can persist, in a milder form, for several months after alcohol discontinuation.

withdrawal seizures can occur anywhere from 0 to 4 days after stopping

alcohol hallucinations can occur 1-4 days after

44
Q

when does delirium tremens develop

A

Delirium tremens typically develops 48–72 hours after alcohol discontinuation.

tachycardia, HTN, fever, tremor, diaphoresis, delirium, agitation

45
Q

treatment of alcohol dependence

A

i) Psychosocial therapy serves as the primary treatment for alcohol dependence
ii) Often depression or anxiety disorders coexist with alcoholism and therapeutic intervention for these other psychiatric problems decreases the rate of relapse

Naltrexone
Acamprosate
Disulfiram

46
Q

Naltrexone

A

(1) Approved for the treatment of alcohol and opiate dependence
(2) MOA: µ opioid receptor antagonist (long-acting)
(3) Reduces the craving for alcohol and the rate of relapse to either drinking or alcohol dependence for the short term (12 weeks)

47
Q

ADR’s of naltrexone

A

(4) Extensive first-pass metabolism; contraindicated in patients with acute hepatitis or liver failure
(5) Causes dose-related hepatocellular injury; avoid combination of naltrexone and disulfiram (also hepatotoxic)
(6) Individuals physically dependent on alcohol and opioids must be opioid-free before initiating therapy because naltrexone precipitates an acute withdrawal syndrome

48
Q

Acamprosate

A

(1) MOA: weak NMDA-receptor antagonist and GABA¬A receptor agonist (also affects serotonergic, noradrenergic, and dopaminergic systems)
(2) Reduces short-term and long-term (more than 6 months) relapse rates when combined with psychotherapy

49
Q

ADR’s of acamprosate

A

(3) Eliminated in urine as an uncharged drug; use caution in patients with kidney disease
(4) Most common adverse effects are nausea, vomiting, diarrhea, and rash
(5) Can be used in combination with naltrexone or disulfiram

50
Q

Disulfiram MOA

A

(1) MOA: irreversibly inhibits aldehyde dehydrogenase and causes extreme discomfort in patients who drink alcoholic beverages (flushing, throbbing headache, nausea, vomiting, sweating, hypotension, confusion due to the accumulation of aldehyde)
(2) Slowly absorbed from GI tract with onset of action from 3-12 hours; little effect of disulfiram alone, but effects described above start within minutes of alcohol consumption and last 30 minutes to several hours; effects may occur when alcohol is consumed up to 14 days after a previous dose

51
Q

ADR’s of disulfiram

A

(3) Hepatotoxic and inhibits the metabolism of other therapeutic agents (phenytoin, oral anticoagulants, isoniazid, caffeine, barbiturates)
(4) Should not be administered with any medications that contain alcohol (cough syrups, cold preparations, mouthwashes)
(5) Not a cure for alcohol dependence and must be used in patients who are highly motivated and have supportive therapy
(6) Never administer to a patient in a state of alcohol intoxication or without patient’s full knowledge
(7) Not commonly used due to low compliance; evidence from clinical trials for its effectiveness is weak

52
Q

ondansetron and alcohol abuse?

A

(a) MOA: antagonizes 5-HT3 receptors
(b) Approved for treatment of nausea and vomiting induced by chemotherapy, radiation, and postoperatively; ongoing clinical trials for reducing alcohol consumption
(c) Preliminary findings suggest that ondansetron is effective in the treatment of early-onset alcoholics who respond poorly to psychosocial treatment alone (early-onset alcoholics are individuals with a severe, lifelong battle with the disease, multiple medical, psychological and social problems, and often a family history of alcoholism)

53
Q

Methanol poisoning

A

i) Poisonings can occur from accidental ingestion of methanol-containing products or when it is used by alcoholics as an ethanol substitute
ii) Most common characteristic symptom in methanol poisoning is blurred vision (“like being in a snowstorm”)

54
Q

how do you treat methanol poisoning

A

iii) Treatment:
(1) Respiratory support
(2) Suppression of metabolism by ADH (ethanol and fomepizole)
(3) Hemodialysis to enhance methanol removal
(4) Alkalinization to counteract metabolic acidosis (bicarbonate)

iv) Ethanol has a higher affinity than methanol for ADH and is often used intravenously as treatment for methanol poisoning
v) Fomepizole inhibits ADH and is approved for the treatment of methanol poisoning

55
Q

ethylene glycol poisoning and treatment

A

b) Ethylene glycol
i) Accidental overdose in pets and children due to the sweet taste of ethylene glycol in antifreeze (also in heat exchangers and industrial solvents)
ii) Metabolized to toxic aldehydes and oxalate
iii) Treatment:
(1) Hemodialysis
(2) Ethanol infusion
(3) Fomepizole

Psych Exam II AP (6 decks)

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