SUDs: Alcohol

Alcohol

CNS depressant

Other CNS depressants

• GHB (date rape drug)

• Ketamine (veterinary anesthetic—-NMDA-receptor antagonist binds to opiate receptors, aka ‘special K’)

Benzodiazepines/Barbiturates

• Ativan, Klonopin, Xanax; Phenobarbital, Rohypnal (date rape drug)

• Sedation and amnestic properties (loss of memories)

• anxiolytics and anticonvulsants

Cannabinoids

Marijuana, Marinol/Dronabinol, THC (active ingredient)

Stimulants

• Nicotine, Caffeine, Methamphetamine/speed, cocaine/crack, Ritalin/Methylphenidate, Ecstasy/MDMA

• stimulant CNS, increase DA

Opiates/Opioids

• Heroin, Methadone, Oxycontin, Oxycodone, Fentanyl

• CNS, resp. depressants

• pain relief, vitals down

• altered memory

• sleepiness

• everything slows (constipation)

Substance Use Disorder

• Correct communication/documentation: (Drug class + use disorder)

• Maladaptive pattern of use

• significant impairment &/or distress

• within 12 month period, 2+ sxs:

  • recurrent use & failure to fulfill major role obligations

  • recurrent use in physically hazardous situations

  • continued use despite social/interpersonal problems for use

  • continued use despite knowledge of problem (psych or physical sxs)

  • craving/strong urge for it

  • Tolerance

  • withdrawal

  • persistent unsuccessful efforts to stop/cut down

  • Bingeing (can cause greater organ damage)

  • great deal of time spent trying to obtain substance

PFC

Suppression of the PFC (normally by a substance or chronic stress) can lead to the strengthening of the emotional and habitual responses of the limbic system (more impulsive) —> reduction of checks and balances for anxiety, impulsivity, focus, memory

Dopamine on developing brains

• children and teens do not have fully developed brains or PFCs so can lead to poor choices

• they crave stimulation (instant AND continuous) from things that deliver DA quickly: devices, substances, games

• Need to be bored time to time to develop PFC’s executive function

Chronic HDA’s (high DA’s)

• continuous release of DA —> PFC de-sensitization (get less effect from DA with same stimuli or activity) —> tolerance (need for more DA to get same effect) over time less endogenous DA release

• “Reward deficiency syndrome”: lack of motivation, anhedonia, depression, ‘seeking’ bxs —> less pleasure/enjoyment in All activities

  • Tx: balance HDA’s and LDA’s, brain breaks, mindfulness

Alcohol Use Disorder

• “Recovery” = lifetime (even if sober many years → recovering alcoholic)

• Little to do with willpower (or the ability to resist temptation) = powerful physiologic cravings (uncontrollable need)

  • One can have motivation, but will not be able to overpower cravings or need for substance = willpower

  • We engage with motivation (via MI and SBIRT strategies + physiological txs)

  • Recovery model: see relapse as part of process & opportunity for progress

Etiology/Risks for AUD

• Children of alcoholics → 3x more likely to develop alcoholism

• Male offspring > females to develop alcoholism

Common comorbidities w/ alcohol use

Pancreatitis and cirrhosis tend to be caused by chronic alcohol use

Physiologic effects of alcohol

• 20% of single dose = absorbed directly to bloodstream thru stomach wall:

  • Absorption varies with:

    • Amount of food in stomach

    • Sipping vs gulping

    • Individual metabolic differences

• Alcohol absorbed faster than metabolized (byproducts build up → effects, toxicity, hangover)

• the more you drink, the longer it takes to metabolize (increased risk of alcohol toxicity)

• CNS and resp. system depressant

Pathophysiology of alcohol

• passes stomach & intestines —> bloodstream to be metabolized by enzymes ADH & ALDH (these convert alcohol to acetaldehyde—toxic byproduct)

• mostly metabolized by liver enzyme

• BAC: small amount of unmetabolized etoh measured in blood, breath, & urine

  • liver can only metabolize a small amount of alcohol per hour

• Metabolic rates partially depend on amount of liver enzymes (ADH & ALDH)

  • some people can also produce less acetaldehyde (aka cause of hangover & genomic deterrant)

Early Alc withdrawal

• Nausea

• Headaches

• Body shakes

Disulfram (Antabuse)

• med deterrent

• increased production of ALDH (facial flushing, nausea, rapid HR)

• less positive response to alcohol = protective vs. alcoholism

• Chinese people and African Americans have genetic variants that lead to low rates of alcohol use (‘Asian flush’)

Alcohol & Teens

• damage to long term and short term growth processes

  • inhibits frontal lobe development

  • NT pathways refinement

  • nerve connections continue to age 16 —> ongoing brain maturity thru mid-20s

• ST or moderate drinking impacts learning & memory in teens

• 50% less alcohol affects teens more dramatically (compared to adults) —> tolerate less alcohol

Teens are increased likelihood use alcohol if:

• parents use: provide (+ or -) for use (socio-cultural-learning mode)

• pleasurable 1st experience (conditioned socio-cultural-behavior response)

Alcohol & Women

• quicker sicker pattern

• women have less H20 in body —> increased ETOH concentrations

• Metabolic hormonal differences

• end-organ damage to heart, liver, brain

• higher risks: breast, liver, rectal, upper respiratory & digestive cancers w/ one drink only

• lower recommended drinking limit

Fetal Alcohol syndrome

• Most common preventable cause of intellectual disability, mental impairment

• Distinctive features:

  • Facial anomalies, low birth weight, heart defects, growth deficits

  • Brain damage: hyperactivity, problems w/ learning, memory, attention, & problem solving (intellectual disability)

  • Brain changes can present even with normal appearances & growth

Alcohol physical effects: short term

• apathy, HA, ataxia (loss of muscle coordination, falls

• decreased balance, judgement, reflexes, coordination, inhibitions

• unconsciousness, coma

• blackouts: amnesia during or immediately after drinking

Alcohol Effect: CNS depressant

• decreases CNS activity in about 10 minutes

• produces morphine like substances in brain

• Increases GABA (inhibitory NT) —> more inhibition —> alcohol tolerance, dependence

• increases DA & 5HT r/t rewards aspects of etoh —> alcohol dependence and tolerance

• Respiratory depressant

Physical effects of alcohol: long term

• high morbidity & mortality r/t loss of coordination, falls

• lowering of inhibitions —> accidents

• respiratory depression, pneumonia, aspiration, overdose (OD)

• alcohol induced depression or anger

• aggravation of mental conditions

Alcoholic Hallucinosis

• hallucinations (mostly visual): ego-dystonic + VH —> tactile & auditory less common

• develop 12-24 hours of abstinence and resolve within 42-48 hrs

• usually normal VS, no other physical sxs

• Pts are aware they are hallucinating (no clouding of sensorium)

Delirium Tremens

• medical emergency

• severe alcohol withdrawal in chronic users and starts 48-96 hrs after last drink (can last 1-5 days)

• 1. Acute delirium: global confusion, disorientation, severe memory disturbance

• 2. Tremors, agitation, hallucinations: paranoia, delusions, nightmares, sense of doom

  • At this point so confused that can’t tell what’s reality even though hallucinations are ego-dystonic

• 3. N/V/D, anorexia, diaphoresis, hyperthermia/fever, tachycardia, HTN

• 4. seizures, dysrhythmias, coma, death (tx: benzos + supportive care: IV fluids, electrolytes, cooling, monitoring)

  • GABA (aka benzos) are anticonvulsants, increase GABA

3rd stage of Delirium Tremens

• N/V/D, anorexia, diaphoresis, hyperthermia/fever, tachycardia, HTN

  • cardiorespiratory instability + increased O2 metabolism —> hyperventilation, resp. alkalosis, decreased cerebral blood flow, electrolyte imbalances, anemias + hypovolemia (from fluid loss)

Wernicke’s Encephalopathy

• sudden, severe brain disorder: acute confusion, muscle loss, ataxia, 6th CN palsy (inability to coordinate voluntary movements), visual changes, nystagmus (rapid, uncontrolled eye movements)

• STM disturbance r/t thiamine deficiency

• leads to Hippocampus damage (aka memory center)

• Emergency tx with thiamine needed to prevent long term brain degeneration (Korsakoff Syndrome)

Korsakoff’s Syndrome

• chronic long term/heavy use of alcohol

• permanent if not prevented early on, cannot create new memories

• Risk groups: male>40, females>30

• progression of Wernicke’s and diagnosed as usually Wernicke-Korsakoff Syndrome

• alcohol = 2nd most neurotoxic drug

Alcohol: Physical & Biological consequences

• Hepatitis (acute or chronic), cirrhosis

  • leading cause of death r/t chronic use of etoh

  • —> encephalopathy, bleeding/clotting problems (upper & lower GI bleeds, esophageal varices), peripheral neuropathy

• pancreatitis

Cirrhosis

• almost exclusively caused by excessive drinking

• fatty deposits and scarring of liver leading to poor liver function and processing of food —> nutrition deficits

• malnutrition is common

• Alcohol both acutely and chronically inflames liver

• chronic inflammation can lead to decreased function of cells and cell death —> cirrhosis

• AST > LFT 2:1 ratio or greater = alcoholic hepatitis

  • If LFT is higher, liver inflammation is higher due to hep A, B,C, etc.

AST and ALT

• liver function tests (how big, leaky, inflamed liver cells are → how hard they are working)

Esophageal Varices from Alcohol

• Liver issue backs up to other systems such as heart

• Portal HTN:

  • As pressure increases, varices can rupture → upper GI hemorrhage (frank hemoptysis) & death

  • High BP in cardiac system → liver already inflamed and have high pressure system in liver from defective blood flow thru cirrhotic liver → backs up to upper system → distended veins (varices=when veins become distended and bulge) → these could burst from coughing, sneezing, etc. and bleed out 

• Not normally candidates for surgery because liver is damaged = bleeding risk

• More so about waiting and cutting back → bring pressures down

Alcoholic Cardiomyopathy

• degenerative changes of heart and skeletal muscles

• CPK elevations (enzyme released when muscle is damaged)

• Acute sxs:

  • sudden onset of extreme muscle pain

  • edema and weaknesses in extremities

  • reddish-tinged urine (caused by myoglobin, a muscle breakdown byproduct excreted in urine)

• Long term:

  • enlarged, floppy

  • less elastic

  • inefficient heart

  • —> HTN, Heart failure

Acute Alcoholic Pancreatitis

• typically occurs 1-2 days after etoh binge

• alcohol use is most common cause

• Signs & sxs:

  • constant, severe left-sided epigastric pain

  • nausea/vomiting

• can become chronic —> affects glucose levels bc pancreas produces insulin

• elevated glucose levels damage blood vessels and nerve endings —> peripheral neuropathy, retinal damage

Peripheral Neuropathy

• peripheral nerve damage r/t long term use of alcohol bc pancreas can no longer control glucose lvls

• Sxs:

  • pain

  • numbness

  • tingling, burning extremities

• believed to be caused by Vitamin B₁ deficiency (Thiamine)

Chronic alcohol effects on skin

• palmar erythema

• spider angioma: microbleeds under the skin d/t clotting complications

• rosacea

• rhinophyma (swelling of nose)

AST

Nml: 0-45 U/L

GGT

Nml: 0-45 U/L

Labs affected by alcohol use disorder

• 2 fold increase in GGT >90 AND

• 2:1 ratio (AST : ALT) strongly suggests alcohol use disorder

• People with extensive/end-stage cirrhosis (aka dead cells) may not show these elevated AST and ALT bc it requires liver to be alive to leak these

  • Need to switch to shorter-acting drugs because longer-acting ones can overdose a patient

3 questions for SUDs assessment

1. What do you use?

2. How much do you use?

3. When was your last use?

Further SUDs assessment

• how often do you use? (frequency)

• how long have you been using? (duration)

• how do you use? (route)

CAGE scale

Screen for alcohol abuse

>2 probable alcohol abuse

Alcohol Withdrawal

• Withdrawal 4-12hrs after last use (cessation or rapid reduction)

• Stage 1 Minor

• Stage 2 severe

• detox (goal)

Stage 1 Alcohol Withdrawal

• 48-72 hrs after last use (r/t increased SNS autonomic output)

• anxiety, agitation, irritability, distractibility, restlessness, shakiness, jitteriness

• tremor, tachycardia, elevated BP, diaphoresis, slight elevated temp (<100.5 F)

• HA, N/V/D, anorexia

• exaggerated startle reflex

• sleep disturbances

Stage 2 Alcohol Withdrawal

• severe, 48-72 hrs after last drink; lasts for 3-5 days

• worsening stage 1 sxs: increased temp, BP/HTN, HR, severe diaphoresis

• defined by presence of hallucinosis (but still cognitively intact

• confusion, disorientation, severe tremors —> seizure, coma, death

Alcohol Detox

• Safety and physiological: prevent withdrawal & associated risks: Seizures (DT’s), complications

• clearing body of substances, regaining equilibrium —> normalizing to baseline neuro-chemistry

• Use benzodiazepines (stimulate GABA)

  • can also cause CNS + resp depression

  • addictive so taper off; stopping suddenly can lead to severe anxiety, seizures, coma, death

Alcohol Withdrawal Syndrome

• Normally alcohol promotes GABA release, an inhibitory NT

• chronic alcohol exposure leads to neuro-adaptation —> down-regulation/decreased GABA receptors WITH up-regulation of NMDA receptors + enhanced sensitivity to glutamate NT’s

• overall effect: neuro-excitation (increased CNS activity) → insomnia, shaking, seizures

• Detox: prevent neuro-excitation: seizures, DT’s, Restore Neuro-balance

Acute Pharmacotherapies: Benzos

• increase GABA to decrease brain excitation / seizure risk

• Taper schedules, never stop suddenly

  • Ativan (Lorazepam)

  • Librium (Chlordiazepoxide)

  • Serax (Oxazepam)

  • Valium (Diazepam)

  • Midazolam (Versed) or Propofol (Diprivan): rarer use

Acute Pharmacotherapies: Alpha-2 adrenergic agonists

• brings VS down, no seizure prevention tho (hence benzos being best)

• Catapres (Clonidine)

  • risks: hypotension, decreases seizure threshold, transdermal or PO only

Acute Pharmacotherapies: beta blockers

• Metoprolol with Gabapentin

Acute pharmacotherapies: anti-psychotic

• Haldol

• decreases AWS severity but need other meds to prevent seizures

CIWA

• Higher doses = worse AWS

• Highest score: 67

• Loading dose = x 0

• Give with Thiamine (IM 1st via loading dose)

• Initiate fall and seizure precautions

• Score: 8-10 mild withdrawal (start meds)

• Score: 10-18 moderate withdrawal

• score: >18 severe withdrawal (increased risk fo DT’s, seizures)

• score 35-67: indicative of need for ICU

Alcohol Emergent Care (ICU)

• severe withdrawal, IV meds required, ongoing monitoring

• Typical inpatient orders:

  • IV w/ multivitamin, thiamine, & folic acid (banana bag)

  • Ativan 1 mg IV PRN (+ BP med to prevent seizures and stabilize vitals)

  • serum electrolytes

  • cooling blanket

  • consistent staff

  • frequent vitals

  • hypoglycemia checks

  • well-lit, quiet room

• Seizure management

seizure management

• provide safety in environments

• assess & document duration

• O2 therapy as needed

• monitor closely after seizure, IV access

• anti-seizure meds administered promptly

Post-Detox Alcohol Pharmacological Tx

• outpatient usually

• Antabuse (Disulfiram)

  • deterrent only

  • 125 mg-500 mg max/day usually in AM

  • start 12-48 hrs after last drink

• Campral (Acamprosate) restores NT balance (GABA activator, NMDA receptor blocker)

• Naltrexone (Revia) reduces cravings

Alcohol Recovery

• relapse is common & normal part of recovery process

  • use as learning tool + ed. r/t importance of stopping again

  • identify triggers + remove/teach avoidance

• Use of MI/SBIRT (screening, brief intervention, and referral to tx)

• emphasize importance of hope & self-determination/individual responsibility

• first step= overcome denial (admit problem)

• referral to support group or 12-step programs