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CMOD Block 2 > Smoking/Alcohol Cessation Therapy > Flashcards

Smoking/Alcohol Cessation Therapy Flashcards

1
Q

Which cessation therapy interventions give the strongest evidence of effect?

A

Advise to quit/avoid second hand smoke

AND

Offer Nicotine replacement therapy/non-nicotine therapy IN COMBINATION with smoking cessation program

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2
Q

Quitting smoking can alter the PKs of what sorts of drugs?

A

antispychotics and antidepressants (CNS drugs)

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3
Q

How does nicotine get absorbed into the body?

A

it is taken up by the alveoli in the lungs

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4
Q

Where does nicotine exert its effects (general)?

A

at specific parasympathetic nicotinic receptors in the brain

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5
Q

In what specific area of the brain are alpha-7, alpha-4, and beta-2 nicotinic receptor conformations located?

A

ventral tegmental area

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6
Q

What action do GABA receptors usually have on dopamine release?

A

they usually inhibit it

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7
Q

What happens with GABA receptors during smoking?

A

the inhibition of GABA receptors on dopamine release is stopped, so increase in dopamine release

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8
Q

How is nicotine addiction related to dopamine?

A

the increased dopamine release (due to GABA inhibition) causes the body to quit producing dopamine naturally–therefore, you must smoke cigarettes in order to get the “feel-good” hormone.

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9
Q

Do the rewarding effects of cigarettes JUST come from dopamine?

A

NO, initial activation of nicotine by GABA neurons in the VTA produces rewarding effects through a GABA-dependent system that projects to the TPP. This is desensitized with prolonged cigarette use (when the dopamine system kicks in).

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10
Q

ALL addictive drugs significantly increase concentration of what in target structures of the mesolimbic projection?

A

dopamine (may be the source of the adaptive changes that underlie dependence and addiciton)

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11
Q

Addictive drugs act on 1 of what 3 targets?

A
  • G proteins
  • Ion channels
  • Amine transporter mechanisms
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12
Q

Nicotine is on par with what type of addictive drug?

A

opiates (less addictive than cocaine but more addictive than alcohol/benzodiazepines)

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13
Q

Describe the nicotine plasma profile of cigarettes.

A

Rapid increase in nicotine

Quick decline

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14
Q

What portion of the nicotine plasma profile of cigarettes is responsible for triggering the physiological changes associated with addiction?

A

rapid increase in nicotine

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15
Q

What portion of the nicotine plasma profile of cigarettes is responsible for onset/severity of the nicotine withdrawal symptoms?

A

quick decline of nicotine

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16
Q

How does nicotine replacement therapy alter the plasma nicotine profile?

A

It produces a sustained plasma nicotine profile that has a slower accumulation to peak levels (avoiding dopamine surge) and a gradual tapering off (avoiding symptoms of withdrawal)

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17
Q

List types of NRT from most effective to least effective.

A

Inhaler/Spray (controversial- low data levels)

Patch and Gum (about equal)

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18
Q

How long do you take most forms of NRT? What is the exception?

A

12 weeks

you take the nicotine nasal spray for 3 months

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19
Q

What are the adverse effects of a nicotine patch?

A

application site reactions
headaches
cold/flu-like symptoms

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20
Q

What should a patient know who wants to use a nicotine patch?

A

DO NOT SMOKE (additive effect)

Do not use if you have CV disease, diabetes, liver problems, etc.

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21
Q

What are the adverse effects of nicotine gum?

A

headache
indigestion
nausea
jaw aches/orodental problems with chewing

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22
Q

What should a patient know who wants to use nicotine gum?

A

Avoid eating/drinking 15 minutes PRIOR to gum

Patient may transfer nicotine addiction to gum

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23
Q

What are the adverse effects associated with nicotine spray/inhaler?

A 
localized irritation of mouth/nostrils
headache
nausea
heartburn
hiccups
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24
Q

What are the top 2 non-nicotine drugs used in cessatiion therapy?

A

Varenicline (Chantix)

Bupropion (Wellbutrin SR)

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25
Q

What is the MOA of varenicline (chantix)?

A
  • Partial agonist of alpha4beta2 nicotinic ACh receptor

- Blocks effect of additional challenge while causing release of mesolimbic dopamine

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26
Q

What are the adverse effects associated with Varenicline (Chantix)?

A
  • Self-limiting nausea
  • Depression, suicidal ideation,and emotional liability
  • CV-related death, nonfatal MI and stroke
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27
Q

What is important to know if your patient is on Varenicline or Bupropion?

A

MUST monitor patient for depression

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28
Q

What is the MOA of bupropion?

A
  • Epinephrine and Norepinephrine re-uptake inhibitor

- Decreases cravings and withdrawal symptoms (like depression)

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29
Q

What are the adverse effects associated with Bupropion?

A
  • Insomnia
  • Dry mouth
  • Nausea
  • Increased risk of suicidal ideation
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30
Q

Which non-nicotine drug would be good for anxious/agitated quitters?

A

Clonidine (Catapres)

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31
Q

What is the MOA of clonidine (catapres)?

A

Oral anti-hypertensive drug that blocks adverse effects of nicotine withdrawal (cravings, anxiety, restlessness, tension, hunger)

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32
Q

What are the adverse effects of Clonidine?

A
  • sedaiton
  • dry mouth
  • dizziness
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33
Q

What non-nicotine drug is used with nicotine replacement therapy to promote cessation?

A

Mecamylamine

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34
Q

What is the MOA of mecamylamine?

A

nicotine antagonist (ganglionic blocker)

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35
Q

What are the adverse effects of mecamylamine?

A

SYMP and PARASYMP AEs:

  • Orthostatic hypotension
  • Fatigue
  • Dry mouth
  • Sedation
  • Constipation
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36
Q

What should you know before you take mecamylamine?

A

NOT for people with coronary or renal insufficiency, glaucoma, or uremia

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37
Q

What is an opiate receptor antagonist that has little use for smoking cessation?

A

Naltrexone (ReVia)

38
Q

What population is NOT supposed to take non-nicotine drugs and could potentially benefit from psychological interventions and NRT?

A

pregnant women

39
Q

What liver enzyme is the first to act on ethanol?

A

alcohol dehydrogenase changes ethanol to acetaldehyde

40
Q

What liver enzyme acts on acetaldehyde?

A

aldehyde dehydrogenase converts acetaldehyde to acetate

41
Q

Why do Native Americans get more pleasure from drinking alcohol?

A

dopamine combines with acetaldehyde to form SALSONLINOL

42
Q

Why do Asians flush when they drink alcohol?

A

they have polymorphisms in their aldehyde dehydrogenase

43
Q

Is alcohol metabolism a first or zero order process?

A

ZERO ORDER (all enzymes are saturated) and a set AMOUNT of alcohol is metabolized per unit time

Dose regulates half-life

44
Q

True or False: CYPs are involved in alcohol metabolism.

A

TRUE: though not much and only in people who are chronic alcoholics

45
Q

How can alcohol intake alter the metabolism of other drugs?

A

it is an important inducer of CYP2E1

46
Q

What drug is especially bad to take if you are a chronic alcoholic?

A

Acetaminophen.

47
Q

Explain the DDI with ethanol and acetaminophen.

A

Acetaminophen is usually conjugated with sulfate or glucuronide

  • A little bit is converted to highly reactive intermediate NAPQI (which is rapidly conjugated and detoxified
  • If you have increased CYP2E1 (chronic alcoholism) you have increased conversion to NAPQI
  • Cannot detoxify NAPQI and it accumulates in liver (hepatotoxicity)
48
Q

How do you treat someone with a DDI from ethanol and acetaminophen?

A

N-acetylcysteine provides fresh conjugate substrate (increased levels of glutathione) for reactive intermediate to be safely detoxified

49
Q

What effect does alcohol have on GABA?

A

causes GABA release

Increases receptor density

50
Q

What effect does alcohol have on NMDA?

A

inhibition of postsynaptic NMDA receptors

upregulation with chronic use

51
Q

What effect does alcohol have on dopamine?

A

increases synaptic dopamine

increases effects on VTA/reward

52
Q

What effect does alcohol have on ACTH?

A

increases CNS and blood levels of ACTH

53
Q

What effect does alcohol have on opiods?

A

release beta endorphins

54
Q

At what BAC do you have “pronounced incoordination”?

A

50-100

55
Q

At what BAC do you have mood and personality changes?

A

100-150

56
Q

At what BAC do you have nausea, vomiting, marked atazia, amnesia, dysarthria?

A

150-400

57
Q

What happens if your BAC increases above 400?

A

coma
respiratory insufficiency
Death

58
Q

True or false: ethanol has a specific receptor in the brain.

A

FALSE. Alcohol does not have a specific receptor int he brain, it modulates key pathways including reinforcement of the inhibitory actions of GABA and inhibition of the stimulatory actions of the glutamate system.

59
Q

What are the acute effects of alcohol?

A 
CV depressant
Relaxation of vascular smooth muscle 
  -Vasodilation
  -Possible hypothermia
  -Increased gastric bloodflow
Relaxation of uterine smooth muscle
60
Q

True or false: larger lean body mass lowers BAL.

A

True (larger total body water volume)

61
Q

True or false: larger BMI lowers BAL.

A

FALSE: smaller volume of distribution because ETHANOL DOES NOT DISTRIBUTE INTO FAT

62
Q

True or false: Female gender increases BAL.

A

TRUE: females have lower body weight, increased absorption and increased % fat

63
Q

True or false: levels of alcohol in fetal blood are higher than maternal blood.

A

FALSE: fetal blood mirrors maternal blood

64
Q

What exactly does ethanol do to cause FAS?

A

triggers apoptosis and incorrect neuronal and glial migration in developing nervous system.

65
Q

Describe what a FAS child looks like.

A 
Microcephaly
Poor coordination
Mid-facial underdevelopment (flattened)
MInor joint anomalies
sometimes congenital heart defects
66
Q

Why would you want to give glucose to an alcoholic patient?

A

You would want to give dextrose to compensate for hypoglycemia

67
Q

Why and when would you want to give an alcoholic patient thiamine?

A

give BEFORE glucose (to prevent worsening of Wernicke-Korsakoff syndrome) because alcoholics are commonly B1 deficient

68
Q

What is your main concern when you have an intoxicated patient?

A

ABCs

69
Q

What is common in withdrawing alcoholics?

A 
insomnia
tremor
anxiety
seizures (rare)
N/V
diarrhea
arrhythmia
70
Q

What can you give a withdrawing patient to sedate them?

A

diazepam

71
Q

What should you give a withdrawing patient (with impaired hepatic function) to sedate them?

A

lorazepam (processed by phase II metabolism only so less susceptible to 1/2 life prolongation

72
Q

What are the effects of chronic alcohol use on the liver?

A
  • decreased gluconeogenesis–> hypoglycemia
  • fatty liver leading to hepatitis, cirrhosis, and liver failure
  • disrupted corticosteroid synthesis
73
Q

What are the effects of chronic alcohol use on the GI tract?

A

bleeding and scarring with absorptive deficiencies

GI cancer increased in alcoholics

74
Q

What are the effects of chronic alcohol use on the endocrine system?

A

gyneocomastia
testicular atrophy
(all secondary to steroid insufficiency)

75
Q

What are the effects of chronic alcohol use on the CNS?

A

Peripheral neuropathy**

Wernicke-Korsakoff (clinical triad: ataxia, confusion 80%, ocular muscle paralysis 30%)

76
Q

What are the effects of chronic alcohol use on the CV system?

A

Hypertension
Anemia
Dilated carciomyopathy
Arrhythmias with binge drinking

77
Q

What are the effects of chronic alcohol use on the immune system?

A

increases inflammation in liver/pancreas
decreases inflammation in all other tissues
susceptible to pneumonia/other infections

78
Q

Name 3 drug treatments for chronic alcoholics.

A

1) Disulfiram
2) Naltrexone
3) Acamprosate

79
Q

What is the MOA of disulfiram?

A

inhibits ALDH with resulting increase in acetylaldehyde after drinking–which makes an adverse reaction that forces abstinence

80
Q

What is the MOA of naltrexone?

A

Opiod antagonist (OP-3) felt to decrease drinking through decreasing feelings of reward with alcohol and/or decrease craving

81
Q

What is the MOA of acamprosate?

A

weak NMDA antagonist, activation of GABAa receptors; may decrease mild protracted abstinence syndromes with decreased feeling of “need” for alcohol

82
Q

What does it mean if a drug has a “disulfiram-like effect”?

A

drugs have ability to increase acetaldehyde in someone who consumes alcohol while taking the drug (for a completely unrelated medical condition)

83
Q

List drugs that cause “disulfiram-like effects”?

A

sulfonylureas
cefotetan
ketoconazole
procarbazine

84
Q

Alcohol exerts its effects through what pathway?

A

cortico-mesolimbic dopaminergic pathway

85
Q

What 2 substances are commonly drank by alcoholics who cannot get access to alcohol?

A

methanol

ethylene glycol

86
Q

Why are methanol and ethylene glycol poisonous?

A

they produce a distinct toxicity due to their conversion to toxic products by alcohol dehydrogenase

87
Q

What drugs may be administered to prevent nephrotoxicity due to methanol and ethylene glycol?

A

Fomepizole

Ethanol

88
Q

What is the MOA of fomepizole?

A

competitive alcohol dehydrogenase inhibitor, administered by IV infusion

prevents initial metabolic conversion of methanol and ethylene glycol leading to their elimination

89
Q

What is the MOA of ethanol?

A

competitive inhibitor of alcohol dehydrogenase, given enough to maintain BAL of 100 mg/dL to ensure enzyme saturation

90
Q

What other methods may be used to mediate the toxicity of methanol and ethylene glycol?

A

induced emesis
gastric intubation/suctioning
absorbent charcol

91
Q

What are the pharmacokinetic DDIs of alcohol and drugs?

A

increased teratogenicity through metabolism

increased absorption of either component

92
Q

What are the pharmacodynamic DDIs of alcohol and drugs?

A
  • additive CNS depression with drugs
  • increased toxicity of acetaminophen
  • increased risk of bleeding with NSAIDs and anticoagulants
  • Increased risk of hypoglycemia in diabetics on medication

CMOD Block 2 (11 decks)

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