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NPB 168 > Alcohol > Flashcards

Alcohol Flashcards

1
Q

Alcohol Structure

A

Ethyl Alcohol
2C chain for consumed alcohol
Carbohydrates

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2
Q

Ethyl Alcohol/Serving

A

0.48-0.5%

Proof = 2x%EtOH

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3
Q

Blood Alcohol Content By Amount Consumed

A 
All are in 95% Concentrations:
15 mL ~ 0.2
30 mL ~ 0.4
60 mL ~ 0.8
* rises faster on an empty stomach due to Alcohol Dehydrogenase (ADH) that lines GI tract
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4
Q

BAC in Men and Women

A

Men’s EtOH BAC vs. Time is generally less dramatic b/c:

1) differences in blood volume
2) differences in gastric metabolism

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5
Q

Alcohol Metabolism

A

Follows zero order kinetics (linear)

Metabolize 6-8g of 100% EtOH/hr (approx. 1 std drink/hr)

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6
Q

Biphasic Effects of Alcohol - Low/Moderate Doses

A 
Behavioral Effects:
Mild stimulation
Mild sedation/sleepiness
Loss of inhibitions/Increased risk taking
Motor in-coordination
Impaired judgment
Loss of emotional control

Physiological Effects:
Vasodilation (feel warm but loosing heat)
Decreased HR, BP and RR
Renal system - more dilute urine
GI tract - irritated GI tract (inflammation)

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7
Q

Biphasic Effects of Alcohol - Higher Doses

A

Magnification of effects listed in low/moderate doses

Memory loss/blackout (can’t form LT memories, EN block, fragmentary)

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8
Q

Dose Dependence of Alcohol

A
  1. 08% - can’t drive
  2. 15% - nausea/vomiting
  3. 35% - lose consciousness
  4. 45% - OD (5.5x legal limit - death due to respiratory depression)
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9
Q

Acute Alcohol Tolerance

A

Feel “sober” but really have a higher BAC than when claimed to be “intoxicated”
** Primary pharmacodynamic

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10
Q

Mi/Long-term Alcohol Tolerance

A

show tolerance when experimental setting drank 1 drink/day for 7 days
Metabolic reasons - primary enzymes are ADH, ALDH and CYP450
See cross tolerance with other sedative-hypnotics

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11
Q

Dependence - Acute (“hangover”)

A 
Approx. 24 hrs
nausea/vomiting
fatigue
thirst
headache
**Dependence of acute toxicity? - residual acetaldehyde, excessive fluid loss, gastric irritation
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12
Q

Dependence - Long-term/chronic use

A

Begins with a couple of hours-last several days
Shakes
Increased BP, HR and RR (can be life-threatening)
Anxiety
Sweating
Nausea/Vomiting

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13
Q

Dependence - Delirium Tremens

A 
Acute withdrawal after long-term use
Sleep disturbances
very disoriented --> hallucinations
Anxiety --> panic attacks
Seizure
Autonomic Distress --> Increased temperature, BP and HR
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14
Q

Long-Term High-Dose Use

A

Wernicke-Korsakoff Syndrome & Brain Damage:

Tremors and other motor problems
Memory dysfunction (short-term memory)
Visual nystagmus
Malnutrition (poor eating habits, poor food absorption through GI tract, leads to significant vitamin and trace element deficiencies particularly with thiamine/B1 which is involved with glucose metabolism)
Cell death - glutamate excitotoxicity and apoptotic cell death (inhibition of glial EAAT1 and 2)

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15
Q

Alcohol-Induced Brain Damage

A

Diet and Hunger - medial thalamus and hypothalamus

Other Deficits
Motor problems - cerebellum
Memory - hippocampus and basal forebrain
Emotion and Affect and Cognitive Skills - Frontal Lobes
Increased Ventricle Size
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16
Q

Beneficial Effects of Alcohol

A

1 drink/day for men

1/2 drink/day for women

17
Q

Effects of Alcohol on the Liver

A

Fatty Liver - get accumulation of triglycerides
Cirrhotic Liver - get necrotic liver (scarred tissue)
- scarring - cuts off transport to tissue (less vascularized) and causes more cell death (get cycle of detrimental effects)

18
Q

Mechanisms of Action - Fluidity and Structure of Membrane

A

Non specific effects

  • disturbs relationship of protein in membrane
  • interacts with polar heads of phospholipids
  • alters lipid composition
19
Q

Mechanisms of Action - Neurotransmitter Receptors

A

Specific Actions

  • acts at NT binding site
  • modifies gating mechanism inside channel
  • stimulates Gs which is linked to adenylyl cyclase
  • direct interaction with channel protein
20
Q

Cellular Effects of Alcohol - Glutamate

A

Acute Effects

  • NMDA receptor antagonist
  • reduces glutamate release

Chronic Use (compensatory response)

  • Increased # of NMDA receptors
  • Increased glutamate release
21
Q

Cellular Effects of Alcohol - GABA

A

Acute Effects

  • GABAa receptor agonist
  • increased Cl influx –> hyperpolarization
Chronic Use (compensatory response)
-  downregulation of GABA-mediated Cl influx --> hyperexcitability and shakes
22
Q

Effects of Alcohol - Dopamine Pathways

A

Increased firing rate of DA-VTA cells –> increased DA release in NAc
Alcohol withdrawal - DA drops with the same time-course that withdrawal symptoms appear
Rats will self-administer EtOH IV or directly into VTA, but if you lesion, DA input into NAc –> decrease but doesn’t abolish self-administration of EtOH

23
Q

Effects of Alcohol - Opiate Pathways

A

Reward is mediated by EtOH’s activation of endogenous opiate circuits
Acute effects
- increased release of endogenous opiates in brain and blood
- increased production of endogenous opiates

Chronic Use: decreased endorphin levels
- opiate antagonists (naloxone/naltrexone) –> reduces self-admin of EtOH

24
Q

Alcohol Withdrawal and Dopamine

A

DORA, DA and HVA concentration levels decrease

Measured by microdialysis - measures extracellular [ ] of a substance

25
Q

Opiate and alcohol reinforcement

A

Mu receptor knockout mice –> less self-administration

shows that Mu opiate pathway is in part responsible for reward

26
Q

Opioid Compensation Hypothesis

A

Deficiency in endogenous opiate activity is compensated by EtOH consumption

EtOH-preferring rats vs. controls

  • increased beta-endorphin release with EtOH administration
  • increased baseline levels of mu-receptors (bigger antenna)
  • EtOH consumption decreases with moderate doses of morphine

Humans (alcoholics and children of alcoholics)

  • lower baseline levels of endogenous species
  • increased release of endogenous opiates with EtOH intake
27
Q

Active and Inactive Alleles of ALDH

A

Asians - 50% have 1 inactive alleles, 10% have 2 inactive alleles
Native Americans - <X inactive alleles, have other alleles that correlated to increased risk of abuse

Inactive alleles of ALDH leads to build up of acetaldehyde which causes vasodilation, nausea, increased HR, headaches, and FLUSHING

28
Q

Fetal Alcohol Spectrum Disorders Symptoms

A 
IQ = 68
Low birth weight with poor catch-up growth
Neurological problems
Increased BP
Irritable/Hyperactive
Attention deficits
Distinct facial malformations
Abnormal development of toes and fingers
Cardio problems
29
Q

Proposed Mechanism for Fetal Alcohol Spectrum Disorders

A

Glutamate-mediated apoptosis and excitotoxicity
Decreased blood flow to fetus via uterine artery
Toxicity of acetaldehyde

NPB 168 (9 decks)

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