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CMOD Block 2 > Smoking/Alcohol Cessation Therapy > Flashcards

Smoking/Alcohol Cessation Therapy Flashcards

(92 cards)

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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
What is the MOA of varenicline (chantix)?
- Partial agonist of alpha4beta2 nicotinic ACh receptor | - Blocks effect of additional challenge while causing release of mesolimbic dopamine
26
What are the adverse effects associated with Varenicline (Chantix)?
- Self-limiting nausea - Depression, suicidal ideation,and emotional liability - CV-related death, nonfatal MI and stroke
27
What is important to know if your patient is on Varenicline or Bupropion?
MUST monitor patient for depression
28
What is the MOA of bupropion?
- Epinephrine and Norepinephrine re-uptake inhibitor | - Decreases cravings and withdrawal symptoms (like depression)
29
What are the adverse effects associated with Bupropion?
- Insomnia - Dry mouth - Nausea - Increased risk of suicidal ideation
30
Which non-nicotine drug would be good for anxious/agitated quitters?
Clonidine (Catapres)
31
What is the MOA of clonidine (catapres)?
Oral anti-hypertensive drug that blocks adverse effects of nicotine withdrawal (cravings, anxiety, restlessness, tension, hunger)
32
What are the adverse effects of Clonidine?
- sedaiton - dry mouth - dizziness
33
What non-nicotine drug is used with nicotine replacement therapy to promote cessation?
Mecamylamine
34
What is the MOA of mecamylamine?
nicotine antagonist (ganglionic blocker)
35
What are the adverse effects of mecamylamine?
SYMP and PARASYMP AEs: - Orthostatic hypotension - Fatigue - Dry mouth - Sedation - Constipation
36
What should you know before you take mecamylamine?
NOT for people with coronary or renal insufficiency, glaucoma, or uremia
37
What is an opiate receptor antagonist that has little use for smoking cessation?
Naltrexone (ReVia)
38
What population is NOT supposed to take non-nicotine drugs and could potentially benefit from psychological interventions and NRT?
pregnant women
39
What liver enzyme is the first to act on ethanol?
alcohol dehydrogenase changes ethanol to acetaldehyde
40
What liver enzyme acts on acetaldehyde?
aldehyde dehydrogenase converts acetaldehyde to acetate
41
Why do Native Americans get more pleasure from drinking alcohol?
dopamine combines with acetaldehyde to form SALSONLINOL
42
Why do Asians flush when they drink alcohol?
they have polymorphisms in their aldehyde dehydrogenase
43
Is alcohol metabolism a first or zero order process?
ZERO ORDER (all enzymes are saturated) and a set AMOUNT of alcohol is metabolized per unit time Dose regulates half-life
44
True or False: CYPs are involved in alcohol metabolism.
TRUE: though not much and only in people who are chronic alcoholics
45
How can alcohol intake alter the metabolism of other drugs?
it is an important inducer of CYP2E1
46
What drug is especially bad to take if you are a chronic alcoholic?
Acetaminophen.
47
Explain the DDI with ethanol and acetaminophen.
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
How do you treat someone with a DDI from ethanol and acetaminophen?
N-acetylcysteine provides fresh conjugate substrate (increased levels of glutathione) for reactive intermediate to be safely detoxified
49
What effect does alcohol have on GABA?
causes GABA release | Increases receptor density
50
What effect does alcohol have on NMDA?
inhibition of postsynaptic NMDA receptors | upregulation with chronic use
51
What effect does alcohol have on dopamine?
increases synaptic dopamine | increases effects on VTA/reward
52
What effect does alcohol have on ACTH?
increases CNS and blood levels of ACTH
53
What effect does alcohol have on opiods?
release beta endorphins
54
At what BAC do you have "pronounced incoordination"?
50-100
55
At what BAC do you have mood and personality changes?
100-150
56
At what BAC do you have nausea, vomiting, marked atazia, amnesia, dysarthria?
150-400
57
What happens if your BAC increases above 400?
coma respiratory insufficiency Death
58
True or false: ethanol has a specific receptor in the brain.
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
What are the acute effects of alcohol?
``` CV depressant Relaxation of vascular smooth muscle -Vasodilation -Possible hypothermia -Increased gastric bloodflow Relaxation of uterine smooth muscle ```
60
True or false: larger lean body mass lowers BAL.
True (larger total body water volume)
61
True or false: larger BMI lowers BAL.
FALSE: smaller volume of distribution because ETHANOL DOES NOT DISTRIBUTE INTO FAT
62
True or false: Female gender increases BAL.
TRUE: females have lower body weight, increased absorption and increased % fat
63
True or false: levels of alcohol in fetal blood are higher than maternal blood.
FALSE: fetal blood mirrors maternal blood
64
What exactly does ethanol do to cause FAS?
triggers apoptosis and incorrect neuronal and glial migration in developing nervous system.
65
Describe what a FAS child looks like.
``` Microcephaly Poor coordination Mid-facial underdevelopment (flattened) MInor joint anomalies sometimes congenital heart defects ```
66
Why would you want to give glucose to an alcoholic patient?
You would want to give dextrose to compensate for hypoglycemia
67
Why and when would you want to give an alcoholic patient thiamine?
give BEFORE glucose (to prevent worsening of Wernicke-Korsakoff syndrome) because alcoholics are commonly B1 deficient
68
What is your main concern when you have an intoxicated patient?
ABCs
69
What is common in withdrawing alcoholics?
``` insomnia tremor anxiety seizures (rare) N/V diarrhea arrhythmia ```
70
What can you give a withdrawing patient to sedate them?
diazepam
71
What should you give a withdrawing patient (with impaired hepatic function) to sedate them?
lorazepam (processed by phase II metabolism only so less susceptible to 1/2 life prolongation
72
What are the effects of chronic alcohol use on the liver?
- decreased gluconeogenesis--> hypoglycemia - fatty liver leading to hepatitis, cirrhosis, and liver failure - disrupted corticosteroid synthesis
73
What are the effects of chronic alcohol use on the GI tract?
bleeding and scarring with absorptive deficiencies | GI cancer increased in alcoholics
74
What are the effects of chronic alcohol use on the endocrine system?
gyneocomastia testicular atrophy (all secondary to steroid insufficiency)
75
What are the effects of chronic alcohol use on the CNS?
Peripheral neuropathy** | Wernicke-Korsakoff (clinical triad: ataxia, confusion 80%, ocular muscle paralysis 30%)
76
What are the effects of chronic alcohol use on the CV system?
Hypertension Anemia Dilated carciomyopathy Arrhythmias with binge drinking
77
What are the effects of chronic alcohol use on the immune system?
increases inflammation in liver/pancreas decreases inflammation in all other tissues susceptible to pneumonia/other infections
78
Name 3 drug treatments for chronic alcoholics.
1) Disulfiram 2) Naltrexone 3) Acamprosate
79
What is the MOA of disulfiram?
inhibits ALDH with resulting increase in acetylaldehyde after drinking--which makes an adverse reaction that forces abstinence
80
What is the MOA of naltrexone?
Opiod antagonist (OP-3) felt to decrease drinking through decreasing feelings of reward with alcohol and/or decrease craving
81
What is the MOA of acamprosate?
weak NMDA antagonist, activation of GABAa receptors; may decrease mild protracted abstinence syndromes with decreased feeling of "need" for alcohol
82
What does it mean if a drug has a "disulfiram-like effect"?
drugs have ability to increase acetaldehyde in someone who consumes alcohol while taking the drug (for a completely unrelated medical condition)
83
List drugs that cause "disulfiram-like effects"?
sulfonylureas cefotetan ketoconazole procarbazine
84
Alcohol exerts its effects through what pathway?
cortico-mesolimbic dopaminergic pathway
85
What 2 substances are commonly drank by alcoholics who cannot get access to alcohol?
methanol | ethylene glycol
86
Why are methanol and ethylene glycol poisonous?
they produce a distinct toxicity due to their conversion to toxic products by alcohol dehydrogenase
87
What drugs may be administered to prevent nephrotoxicity due to methanol and ethylene glycol?
Fomepizole | Ethanol
88
What is the MOA of fomepizole?
competitive alcohol dehydrogenase inhibitor, administered by IV infusion prevents initial metabolic conversion of methanol and ethylene glycol leading to their elimination
89
What is the MOA of ethanol?
competitive inhibitor of alcohol dehydrogenase, given enough to maintain BAL of 100 mg/dL to ensure enzyme saturation
90
What other methods may be used to mediate the toxicity of methanol and ethylene glycol?
induced emesis gastric intubation/suctioning absorbent charcol
91
What are the pharmacokinetic DDIs of alcohol and drugs?
increased teratogenicity through metabolism | increased absorption of either component
92
What are the pharmacodynamic DDIs of alcohol and drugs?
- 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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