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Adv Pharm 1 > Neuro (pt 2/4) Alcohol > Flashcards

Neuro (pt 2/4) Alcohol Flashcards

1
Q

-A sedative-hypnotic with low potency– relieves anxiety and fosters a state of well-being or possibly euphoria at low to moderate amounts
-Most commonly abused drug in the world
-8% of the general population of the USA has an alcohol-use disorder

A

Alcohol

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2
Q

What is Alcohol abuse?

A

Utilization of alcohol in dangerous situations (drinking & driving) or continuing to drink alcohol in spite of adverse consequences directly related to their alcohol consumption

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3
Q

What is Alcohol Dependence?

A

Definition of abuse plus tolerance to alcohol and signs and symptoms of withdrawal; inability to control consumption, obtaining and consuming alcohol is a primary purpose

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4
Q

A small water-soluble molecule that is absorbed rapidly from the GI tract.

A

Ethanol

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5
Q

Describe peak concentrations of Ethanol for men vs women.

A

Peak concentrations are reached within 30 minutes.
-Peak within the CNS happens quickly b/c the brain receives a large proportion of total blood flow
-Women peak concentrations faster than men for equivalent consumption due to having a lower total body water content, and differences in 1st pass metabolism.

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6
Q

Where is Ethanol oxidized/excreted?

A

-90% oxidized in the Liver.
Remainder is excreted through the lungs and in the urine

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7
Q

A family of cytosolic enzymes that catalyze alcohol to acetaldehyde.
-Genetic variation in ADH enzymes that affect the rate of ethanol metabolism and alter vulnerability to alcohol disorders

A

Alcohol dehydrogenase

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8
Q

How does Alcohol Dehydrogenase metabolize Ethanol?

A

Alcohol dehydrogenase uses NAD as a cofactor.
-Hydrogen ion is transferred to cofactor, get NADH.
-Ethanol is metabolized to acetaldehyde.

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9
Q

How does the Microsomal Ethanol-Oxidizing system (MEOS) metabolize Ethanol?

A

-Uses NADPH as a cofactor in metabolism of ethanol.
-Consists of CYP enzymes.
-During chronic alcoholism, MEOS activity is induced, and increased metabolism of any substance that is reliant on CYP 450.

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10
Q

What is the end product of Ethanol metabolism by Alcohol Dehydrogenase or MEOS?

A

Acetaldehyde (not final step though)

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11
Q

Where is Acetaldehyde metabolized?

A

End product of Ethanol metabolism is acetaldehyde, which is oxidized in the liver to acetate.
-Acetate is further metabolized to CO2 and water, or used to form Acetyl-CoA.

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12
Q

What drug inhibits alcohol dehydrogenase?

A

Fomepizole

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13
Q

What enzyme converts Acetaldehyde to Acetate?

A

Aldehyde dehydrogenase

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14
Q

What drug inhibits aldehyde dehydrogenase?

A

Disulfiram

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15
Q

How does Disulfiram deter drinking in chronic drinking or dependence?

A

Buildup of acetaldehyde leads to facial flushing, nausea, sick, etc. Negative feedback deters activity.

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16
Q

A drug that inhibits aldehyde dehydrogenase, so alcohol is metabolized as usual, but acetaldehyde accumulates.
-Rapidly absorbed, elimination is slow (several days)
-Small increases in LFTs
-Teratogenicity unknown
-Causes extreme discomfort in patients who drink alcoholic beverages

A

Disulfiram

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17
Q

Disulfiram inhibits the metabolism of what other drugs?

A

-Phenytoin, oral anti-coags, isoniazid
-Should not be given with other meds that contain alcohol

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18
Q

What are S/sx of a Disulfiram reaction?

A

-Flushing, throbbing headaches, N/V, sweating, hypotension, and confusion
-Lasts 30 min in mild cases and several hours in severe cases

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19
Q

A Long acting opioid receptor antagonist
-Blocks the effects at the mu opioid receptors (blocks happy effects from alcohol)
-Inhibits self administration of alcohol
-PO or IM
-Dose-dependent hepatotoxicity
-Do not administer with Disulfiram
-Adherence is favorable for relapse prevention and tx of alcohol depdendence.

A

Naltrexone

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20
Q

T/F: You can administer Naltrexone to patients with opioid dependence.

A

FALSE; do not admin to pts with opioid dependence

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21
Q

A drug utilized in Europe for the treatment of alcoholism. Did not show statistically significant effects alone or in combo with Naltrexone

A

Acomprosate

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22
Q

What other meds are used Off Label to reduce cravings in chronic alcoholism?

A

-Ondansetron (Zofran)
-Topiramate (Topamax)
-Baclofen

23
Q

How do you treat Alcohol Withdrawal?

A

Motor agitation, insomnia, and reduction of seizure threshold

24
Q

What are the S/sx associated with Alcohol Withdrawal at 6-8 hours?

A

Increased BP, tremor, anxiety, and insomnia
-Usually lessens after 1-2 days

25
Q

What are you at risk for from 1-5 days of Alcohol Withdrawal?

A

Risk of seizures and hallucinations

26
Q

Anxiety and sleep disturbances associated with Alcohol Withdrawal can persist for ______.

A

Several months

27
Q

When do DT’s begin?

A

48-72 hours after alcohol cessation
Can last 5-10 days

28
Q

What are the symptoms of Delirium Tremons (DT’s)?

A

Delirium, agitation, ANS instability, low-grade fever, diaphoresis

29
Q

What is the drug therapy for Alcohol Withdrawal?

A

-Correct electrolyte imbalances (K, Mg, Phos)
-A long acting sedative-hypnotic (Benzos) - such as Chlordiazepoxide (Librium) or Diazepam (Valium)

30
Q

A patient with decreased Liver Function and is experiencing acute alcohol withdrawal requires the use of____?

A

-Due to the active metabolites of benzos in the presence of compromised liver function, you should use a short-acting Benzo in a patient with Liver Dz.
-Lorazepam (Ativan)
-Oxazepam (Serax)

31
Q

What are the CNS effects of Acute Alcohol Consumption?

A

Sedation
Relief of anxiety
Slurred Speech
Ataxia
Impaired judgment
Disinhibited behavior
Tolerance develops after a couple of hours

Alcohol is a CNS depressant that affects a large number of membrane proteins.

32
Q

What are the CNS effects of Chronic Alcohol Consumption?

A

-Dementia
-Withdrawal is associated with seizures, toxic psychosis DT’s
-Wernicke-Korsakoff Syndrome
-Bilat symmetric impaired visual acuity with painless blurring – leading to optic nerve degeneration

33
Q

What is the effect of acute alcohol intoxication of neurotransmitters (GABA and Glutamate)?

A

-Enhances action of GABA at GABA Alpha Receptors (GABA Alpha antagonists can attenuate some of alcohols effects)
-Blocks glutamate action on the NMDA receptor (reason for why people black out)

34
Q

What is the effect of Chronic Alcohol consumption on tolerance and physical/psychological dependence?

A

-A limit to tolerance so that only a small increase in lethal dose occurs with increased use
-Tolerance may result from up-regulation of neural pathway and Dependence may result from over activity of that same pathway after ethanol dissipates

35
Q

What is Wernicke-Korsakoff Syndrome?

A

-Paralysis of the external eye muscles, ataxia, and confusion that can progress to coma and death
-Rare
-Caused by Thiamine deficiency
-A complication of chronic alcohol consumption

36
Q

What is the effect of Chronic Alcohol Consumption on the Peripheral Nervous System?

A

-Generalized symmetric peripheral nerve injury
-Distal paresthesias of hands and feet
-Degenerative changes resulting in gait disturbances and ataxia

37
Q

What is the effect of Acute Alcohol Consumption on the CV system?

A

-Significant depression of myocardial contractility at BAC > 100mg/dl
-Vasodilation 2/2 CNS effects (depression of the vasomotor center) and direct smooth muscle relaxation of its metabolite (acetaldehyde)
-Vasodilation can be marked in cold environments

38
Q

What is the effect of Chronic Alcohol Consumption on the CV system?

A

-Dilated cardiomyopathy
-Ventricular hypertrophy
-Fibrosis
-Ethanol interferes with the therapeutic effects of beta blockers
-Atrial and ventricular arrhythmias
-HTN
-Prevents CAD 2/2 ethanol’s ability to raise HDL

39
Q

What is the effect of Acute Alcohol Consumption on the Reproductive system?

A

Relaxes the uterus and was once used IV to suppress premature labor

40
Q

What is the effect of Chronic Alcohol Consumption on the Reproductive system?

A

-Gynecomastia
-Testicular atrophy
-Leading cause of mental retardation and congenital malformation (fetus cannot metabolize ethanol)
-Fetal Alcohol Syndrome – ethanol crosses the placenta and the fetus must rely on mom’s enzymes for elimination

41
Q

What is the effect of Chronic Alcohol Consumption on the GI system?

A

-Liver disease is the most common complication
-Women are more susceptible to hepatotoxicity than men
-Tumor necrosis factor-α (proinflammatory cytokine) plays a significant role in alcohol associated liver disease
-Common cause of chronic pancreatitis (Alcoholism promotes the formation of protein plugs and calcium carbonate stones)
-Gastritis
-Small intestine damage (D, wt loss & MVI deficiencies)

42
Q

What is the effect of Chronic Alcohol Consumption on the Blood?

A

-Mild anemia related to folic acid deficiency
-Iron deficiency anemia may result from GI bleed
-Implicated as a cause of several hemolytic syndromes

43
Q

What is the effect of Chronic Alcohol Consumption on the Endocrine System & Electrolytes?

A

-Disruption in steroid hormone balance
-Ascites, edema, and effusions
-Hypoglycemia
-Ketosis

44
Q

Other misc. effects of Chronic Alcohol Consumption on the body

A

-Organ & tissue damage r/t the direct effects of ethanol and acetaldehyde and the metabolic consequences of a marked amount of metabolic byproducts
-Increased oxidative stress
-Depletion of glutathione (Avoid Tylenol!!!)
-Damage to mitochondria
-Growth factor dysregulation
-Potentiation of cytokine induced injury
-Associated with increase infections, especially of the lungs and increase the M&M of pts with pneumonia
-Increases the risk of cancer of the mouth, pharynx, larynx, esophagus and liver r/t metabolites

45
Q

Alcohol can potentiate the effects of many nonsedative drugs including _____ & ______.

A

vasodilators and oral hypoglycemics

46
Q

T/F: Alcohol has an additive effect with sedatives/hypnotics

A

True

47
Q

Acute alcohol consumption requires ____ anesthesia, while chronic consumption requires _____.

A

Less; more

48
Q

Expect _____ on induction for both acute and chronic alcohol consumption due to vasodilation.

A

Hypotension

49
Q

Acute consumption of alcohol inhibits the metabolism of what other drugs due to decreased enzyme activity or decreased liver blood flow?

A

-Phenothiazine
-Tricyclic antidepressants
-Sedative-hypnotics

50
Q

Prolonged (chronic) alcohol intake without liver damage can _____ the metabolism of other drugs.

A

enhance

51
Q

T/F: Acetaminophen metabolism is greatly affected by ethanol mediated increases in CYP activity

A

True

52
Q

Why does the risk of hepatotoxicity increase from acetaminophen use with alcohol use?

A

Consumption of 3 or more alcoholic drinks/day increases the risk of hepatotoxicity from therapeutic high or toxic levels of acetaminophen, due to acetaminophen’s hepatotoxic metabolites (glutathione depletion)

53
Q

Describe the different Blood Alcohol Concentrations and their Clinical Effects.

A

50-100: Sedation, subjective “high”, slower rxn time
100-200: impaired motor function, slurred speech, ataxia
200-300: emesis, stupor
300-400: coma
>400: respiratory depression, death

54
Q

T/F: You would want to induce alcohol intoxication patient with RSI and Cricoid Pressure

A

True

Adv Pharm 1 (28 decks)

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