Alcohol Flashcards

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1
Q

Describe the absorption of alcohol

A
  • Orally admin, and absorbed in the digestive tract, especially from the small intestine.
  • Molecules not ionizable; hence digestive system pH and blood pH have no effect on absorption.
  • Some of the alcohol destroyed by alcohol dehydrogenase (ADH) in the stomach; known as First pass metabolism (FPM)
  • Solid food in the stomach slows the absorption of alcohol.- it does not reduce amount absorbed
  • There also appears to be a gender difference in FPM. Women appear to have lower levels of ADH in their stomachs than men.
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2
Q

Describe the metabolism of alcohol

A
  • 90-98% metabolized in liver
    • Alcohol dehydrogenase
      - ACETATE
    • Aldehyde dehydrogenase
      - Acetaldehyde
  • Alcohol dehydrogenase saturates at low to moderate BACs (Michaelis-Menten kinetics)
  • Apparent zero-order kinetics at moderate BACs
    • Alcohol Elimination Rate = 9 g per hr
    • Disappearance Rate = 0.015g(per 100ml blood)% per hr

Where is it metabolised
- liver, but also lungs, kidneys
- liver= hence breathalyser

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3
Q

Describe the neuropharmacology of alcohol

A
  • Alcohol does not seem to have its own specific receptors to which it binds.
  • No competitive antagonist have been found yet.
  • The alcohol molecules may act directly on the receptor sites of many NTs and the ion channels they control, thereby altering the effects of the transmitter.
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4
Q

What are some physical exam signs?

A
  • Physical features (heavy alcohol users)
    • Elevation in blood pressure
    • Irregular heart rhythms or tachycardia
    • Enlarged liver/spleen
    • Extremities -myopathy, neuropathy
  • Other rarer features
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5
Q

What are some clues based on past medical history?

A
  • Recurrent trauma
  • Pancreatitis, GE reflux, dyspepsia, gastritis
  • Fatty liver, alcoholic hepatitis, cirrhosis
  • Hypertension, cardiomyopathy, arrhythmias
  • Dementia, cerebellar disease, peripheral neuropathy, Wernicke-Korsakoff syndrome
  • Dupuytren’s contractures
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6
Q

List some medical complications of AUD

A
  • Gastroenterological eg alcoholic gastritis and oesophagitis, alcoholic pancreatitis, alcohol iver disease eg fatty liver, alcohohlic hepatitis, cirrhosis; cronic diarrhoea
  • Neurological eg blackouts, W-K syndrome, peripheral neuropathy, cerebral atrophy, cerebellar degeneration, pseudo-Parkinsonism , subdural haematoma
  • Haematological eg anaemia, thrombocytopenia, leukocytosis
  • Endocrine and metabolic eg sexual dysfunction, pseudo-Cushing Syndrome, diabetes mellitus, hyperuricaemia, diabetic ketoacidosis
  • Cardiovascular eg CM, dysrhythmias, hypertension, haemorrhagic CVA
  • Infectious eg pneumonia, spontaneous bacterial peritonitis
  • Malignant
  • Other
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7
Q

Describe blood tests for alcohol use

A
  • For recent consumption
    • Blood alcohol
  • For “chronic” consumption
    • GGT, AST, ALT, MCV, CDT
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8
Q

Recall the CAGE questionnaire and AUDIT

A
  • CAGE Questionnaire
    • Have you ever felt you ought to - Cut down on your drinking? -
    • Have people - Annoyed you by criticizing your drinking?
    • Have you ever felt bad or - Guilty about your drinking?
    • Have you ever had a drink first thing Eye-opener? in the morning to steady your nerves or to get rid of a hangover
  • Two “yes” answers correctly identify 75% of problem drinkers. Three “yes” answers raises this specificity to over 95%.

alternatively alcohol audit screen

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9
Q

Describe who brief interventions are for

A
  • Effective for hazardous drinking. These are simple, short pieces of advice.
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10
Q

Describe Ledermann curve

A
  • A continuum of drinking - no separate cohort
  • The observation by Ledermann that the frequency distribution of alcohol consumption in the population of consumers may be log-normal; the curve is sharply skewed—approximately one-third of drinkers consume more than 60% of the total amount of alcohol.
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11
Q

Define substance use disorder

A

A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by 2 or more of the following occurring within 12 mo

  • The severity of the disorder will be graded by the number of criteria the person meets. If it’s 0 to 1, no diagnosis is made. From 2 to 3 criteria, the diagnosis is mild; 4 to 5, moderate; and 6 or more, severe.
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12
Q

Describe some alcohol induced liver diseases

A
  • Fatty liver
    • Benign and reversible
  • Alcoholic hepatitis
    • Severe cases rare but life threatening
  • Cirrhosis
    • Largely irreversible
    • 15% persons drinking 150g/d for 10+ yrs
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13
Q

imp

Describe thiamine deficiency

A
  • Thiamine, also known as vitamin B1, is an essential nutrient required by all tissues.
  • The human body cannot produce thiamine.
  • Thiamine-rich foods include meat and poultry; whole grain cereals, nuts, dried beans, peas, and soybeans.
  • A daily intake of 1.1 mg is currently recommended.
  • Thiamine is required for several enzymes for carbohydrate catabolism. These are required for critical biochemical reactions in the body, including the synthesis of neurotransmitters, nucleic acids, and production of fatty acids, steroids, and complex sugar molecules. The cells of the nervous system and heart seem particularly sensitive to the effects of thiamine deficiency0
  • Triad= confusion, ophthalmoplegia and ataxia.

Alcohol’s Effects on Thiamine Uptake and Function

Research has identified several mechanisms through which alcoholism may contribute to thiamine deficiency. The most important of these mechanisms (Hoyumpa 1980) include:
- Inadequate nutritional intake
- Decreased absorption of thiamine from the gastrointestinal tract and reduced uptake into cells
- Impaired utilization of thiamine in the cells.

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14
Q

What is deficiency of B1 implicated in?

A
  • Wernicke’s encephalopathy
  • Korsakoff Psychosis
  • Cerebellar Degeneration
  • Alcoholic Polyneuropathy
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15
Q

Describe the nutritional impact of alcohol

A
  • Protein – 4 Calories per gram
  • Carbohydrate – 4 calories per gram
  • Fat – 9 calories per gram
  • Alcohol - 7 calories per gram

Despite the “abundance” of calories available from alcohol, many heavy drinkers are in reality nutritionally deficient. Particularly:
- Vitamins B1, B6
- Protein
- Folate
- Vitamins A, C, B12
- Mg+ Zn, Fe, Ca, PO4

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16
Q

What is the impact of neuroscience on our view of AUD?

A
  • Biological mechanisms were identified and increasingly understood.
  • Neural pathways in the mid-brain concerned with reward and reinforcement.
  • Dopamine release as the final common pathway for the actions of multiple addictive substances.

The Impact of Genetic Studies

There has been a huge increase in our understanding of the genetic basis of substance dependence:
- Biometrical genetic studies (twin, adoption)
- Genome mapping (QTL studies)
- Identification of genetic variants associated with predisposition to dependence
- Significant polygenic influences on substance dependence

17
Q

Describe factors contributing to vulnerability to develop a specific addiction

A

Genetic | (25-50%)- DNA, SNPs, other polymorphisms |
| ————- | ————————————————————————– |
| Environmental | (very high)- prenatal, postnatal, contemporary, cues, comorbidity |
| Drug-Induced | (very high)- mRNA levels, peptides, proteomics; neurochemistry, behaviours |

18
Q

Describe the treatment structure for alcohol use disorder

A
  • “Detox” is not always needed
  • Several forms of rehab
    • Short-term inpatient
    • Outpatient drug-free
    • Long-term residential
    • Outpatient maintenance
    • Aftercare
19
Q

What are te main elements of alcohol use disorders tratement?

A
  1. Set abstinent drinking goal.
  2. Treat alcohol withdrawal.
  3. Treat medical complications.
  4. Refer patient to inpatient or outpatient treatment program and mutual-aid group, e.g., Alcoholics Anonymous.
  5. Discuss family treatment (e.g., AlAnon).
  6. Consider pharmacotherapy (e.g., naltrexone).
  7. Treat concurrent mental illness.
  8. Provide ongoing support to patients and their families.
20
Q

What are some medications for relapse prevention of AUD>

A
  • Naltrexone (1994)
  • Disulfiram (1950)
  • Acamprosate
21
Q

Describe how to communicate with the patient

A

mmunicating with the Patient

  • Give him or her the diagnosis.
  • Explain that she/he is suffering from an illness, not from a moral weakness or lack of will power.
  • Discuss your concerns about his/her health and social situation.
  • Explain that the illness is treatable and you can help.

Principles of Motivational Interviewing

  • Patients are in different stages of “readiness to change”:
    • Precontemplation
    • Contemplation
    • Action
  • Most patients are ambivalent, weighing the pros and cons of changing vs not changing.
  • Encouraging patients to explore their ambivalence may lead to resolution and commitment to change.
22
Q

Describe alcohol withdrawal

A

Alcohol withdrawal
- dangerous
- tachycardia
- anxiety
- tremor
- hypertension
- severe has high mortality if untreated
- treated with benzodiazepines (more in year 4)

Salient Points

  • Alcohol withdrawal remains dangerous, and is still associated with morbidity and potential mortality.