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BPS > Kruse DSA: Pharmacology of Alcohol > Flashcards

Kruse DSA: Pharmacology of Alcohol Flashcards

1
Q

Drugs we use for the tx of acute alcohol withdrawal syndrome

A
  • Diazepam
  • Lorazepam
  • Oxazepam
  • Thiamine
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2
Q

Drugs for the prevention of alcohol abuse

A
  • Acmprosate
  • Disulfiram
  • Naltrexone
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3
Q

Drugs for the tx of acute methanol or ethylene glycol poisonin

A
  • Ethanol

- Fomepizole

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4
Q

What is fetal alcohol syndrome

A

-a syndrome of craniofacial dysmorphia, heart defects, and mental retardation caused by the teratogenic effects of ethanol consumption during pregnancy

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5
Q

Wernicke Korsakoff syndrome

A

-syndrome of ataxia, confusion, and paralysis of the EO muscles that is associated with chronic alcoholism and thiamine deficiency

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6
Q

Where does alcohol get absorbed the most?

A

-the small intestine

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7
Q

What order kinetics does alcohol follow?

A
  • zero order

- independent of time and concentration

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8
Q

What enzyme metabolizes alcohol?

A
  • Alcohol dehydrogenase (ADH)

- aldehyde dehydrogenase (ALDH)

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9
Q

What does fomepizole inhibit

A

-alcohol dehydrogenase

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10
Q

What does disulfiram inhibit?

A
  • Aldehyde dehydrogenase

- gives you a bitch of a hangover

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11
Q

What does ADH do?

A
  • converts ethanol to acetaldehyde

- in the liver

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12
Q

What other thing is required to vonvert ethanol to acetaldehyde?

A
  • NAD+

- so, NADH comes out of there too

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13
Q

What does aspirin do in this DSA?

A
  • inhibits gastric ADH and can increase ethanol bioavailability
  • Fomepizole inhibits ADH and is used in tx of acute methanol or ethylene glycol poisoning
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14
Q

What is acetadehyde also dependent on?

A

-NAD+

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15
Q

What does acetaldehyde get converted to?

A
  • acetic acid

- (produces NADH)

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16
Q

Which drug inhibits ALDH?

A

-disulfiram, a drug used for the tx of alcohol abuse and dependence

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17
Q

does ALDH have genetic polymorphisms?

A
  • yes

- Asians… remember Ross the boss tanaka

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18
Q

What is the microsomal ethanol oxidizing system (MEOS)?

A
  • oxidases (CYP450’s) use NADPH as a cofactor in the metabolism of ethanol to acetaldehyde
  • higher concentrations of alcohol
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19
Q

Which cyp does chronic alcoholism induce?

A
  • CYP2E1

- enhanced activation of toxins, free radicals, and hydrogen peroxide

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20
Q

What big ion channel does ethanol affect?

A
  • NMDA subtype of glutamate receptors
  • glutamate= primary excitatory NT in CNS
  • GABA receptor… inhibitory in CNS
  • enhances effects of GABA receptor and leads to an increased depression of the CNS
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21
Q

What is the most common cause for both acute and chronic pancreatitis in the US?

A

-Alcohol

22
Q

Why do alcoholics get fatty liver?

A

-inhibition of both the TCA cycle and the oxidation of fat…. owing to the generation of excess NADH produced

23
Q

What is tolerance

A

-reduced behavioral or physiological response to the same dose of ethano

24
Q

What is that severe sign of alcohol withdrawal?

A

-delirium tremens

25
Q

What is Wernicke-Korsakoff syndrome?

A
  • paralysis of the EO muscles, ataxia, and a confused state that can progress to coma and death
  • Associated with thiamine deficiency and rarely seen in the absence of alcoholism
  • Tx with thiamine will improve ovular problems, ataxia, and confusion, but most pts are left with a chronic disabling memory disorder known as Korsakoff’s psychosis
26
Q

What did studies show about alcohol and CHD?

A

-moderate alcohol consumption prevents CHD and reduces mortality more than in ppl who abstain or are heavy consumers or alcohol

27
Q

Why do chronic drinkers have mild anemia

A

-folic acid deficiency

28
Q

Why the iron deficiency anemia?

A

-GI bleeding

29
Q

What is the weird thing that happens with body temp

A

-due to increased cutaneous and gastric blood flow, sweating may occur while the internal body temp falls

30
Q

Why would someone going through withdrawal experience hyponatremia?

A

-vasopressin release is increased during withdrawal… so they retain a shit ton of water

31
Q

What is the leading cause of mental retardation and congenital malformation ?

A

-Alcohol

32
Q

What all comes with the Fetal alcohol syndrome package?

A
  • Intrauterine growth retardation
  • Microcephaly
  • poor coordination
  • underdevelopment of midfacial region
  • minor joint abnormalities
33
Q

Does the fetal liver have alcohol dehydrogenase activity?

A

-nah

34
Q

What enzyme levels are increased from chronic ethanol consumption?

A
  • CYP450s
  • particularly, CYP2E1
  • acetaminophen will fuck these people up
35
Q

What do we do to manage acute alcohol intoxication?

A
  • prevent severe resp depression and aspiration of vomitus
  • Glucose can tx metabolic things like hypoglycemia and ketosis
  • Thiamine to protect against the Wernicke-Korsakoff syndrome
  • Potassium may be needed in the event of severe vomiting
36
Q

What drug can we give them if they are having a really bad withdrawal?

A
  • long acting benzos (diazepam)
  • less frequent dosing and built in tapering effect
  • but watch out for pts with a compromised liver because then pharmacologically active metabolites may accumulate
37
Q

What do we do for someone in withdrawal but they’re liver function sucks?

A
  • give them a short acting benzo like lorazepam or oxazepam

- rapidly converted to inactive metabolites and are useful in pts with liver disease

38
Q

What is Naltrexone?

A
  • approved for tx of alcohol and opiate dependence
  • MOA: mu opioid receptor antagonist (long acting)
  • reduces craving for alcohol and the rate of relapse to either drinking or acohol dpendence for the short term
39
Q

When is Naltrexone contraindicated?

A

-in pts with acute hepatitis or liver failure

40
Q

What do we have to make sure the patient is clear of before we give them Naltrexone?

A
  • must be opioid-free!!!!!

- Naltrexone will create an acute withdrawal syndrome

41
Q

Acamprosate

A
  • MOA: weak NMDA receptor antagonist and GABAa receptor agonist
  • Reduces short-term and long-term relapse rates
  • elminated in urine as an uncharged drug; use caution in patients with kidney disease
  • can be used in combo with naltrexone or disulfiram
42
Q

Disulfiram

A
  • MOA: irreversibly inhibits aldehyde dehydrogenase and causes exteme discomfort in pts who drink alcoholic beverages
  • Slowly absorbed from GI tract with onset of action from 3-12 hrs; effects may persist up to 14 days from previous dose
  • hepatotoxic, inhibits metabolism of other therapeutic agnets
43
Q

What should we not mix disulfiram with?

A

-other drugs that contain alcohol

44
Q

What is the caveate with disulfiram?

A

-the pts must be highly motivated and have supportive therapy

45
Q

should we give disulfiram in a state of alcohol intoxication?

A

-no!

46
Q

What is the most common characteristic symptom in methanol poisoning ?

A

-blurred vision (like being in a snowstorm)

47
Q

tx of methanol poisoning

A
  • resp support
  • suppression of metabolism by ADH (ethanol and fomepizole)
  • Hemodialysis to enhance methanol removal
  • alkalinzation to counteract the metabolic acidosis (bicarb)
48
Q

Which has a higher affinity for ADH, methanol or ethanol?

A
  • ethanol actually, that is why you give them a drink lol

- remember fomepizole inhibits ADH and is approved for the tx of methanol poisoning

49
Q

What is ethylene glycol metabolized to?

A

-toxic aldehydes and oxalate

50
Q

Tx for ethylene glycol

A
  • hemodialysis
  • ethanol infusion
  • Fomepizole

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