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Pharmacology 2 > 2.1 Ethanol > Flashcards

2.1 Ethanol Flashcards

1
Q

Most commonly abused substance in the world is

A

ethanol

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2
Q

durgs with similar ethanol actions

A

barbiturates or benzodizepines

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3
Q

Pharmaco dynamics/pharmacological effects of acute ethanol consumption on CNS

A

like anesthetics, when alcohol is consumed,
cortex and RAS are depressed which are
areas that exhibit control over the body
–> causes apparent excitement, but is NOT a stimulant
–>inhibition of inhibition.
Hyperactivity occurs due to removal of inhibitory effects

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4
Q

Ethanol causes CNS depression by

A

enhancing GABA stimulated influx of chloride through receptor gated membrane ion channesl (GABAmimetic effect),

inhibits NMDA receptors

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5
Q

Ethanol affects a lare number of membrane proteins that participate in signaling pathways such as

A 
NT receptors for 
AA and opiodes, 
enzymes such as Na/K ATPase, 
adenylcyclae, 
PLC, 
ion channels
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6
Q

ethanol causes euphoria by

A

enhancing endorphin production

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7
Q

ethanol reduces both mental and physical efficiency, and as level in plasma increases, person develps

A

there are more drunk person effects

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8
Q

high dose ethanol

A

analgesia,
anesthesia,
sleep

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9
Q

toxic dose ethanol

A 
person becomes unconscious and alcohol depresses medullary center, 
causing death (due to respiratory depression)
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10
Q

thymine deficiency due to poor diet and dec absorption by acetaldehyde and chronic alcoolism leads to

A

Wernicke-Korsakoff syndrome

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11
Q

ethanol causes peripheral vasodialation by

A

depression of VMC (direct), by relaxation of smooth muscle caused by its metabolite (acetaldehyde) feeling of warmth followed by inc in body heat loss

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12
Q

ethanol causes diuretic effect by

A

inhibiting secretion of ADH

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13
Q

gastric mucosa and small dose of ethanol

A

stimulates salivary secretions,
gastric secretions,
improves appetite – appetizer

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14
Q

gastric mucosa and high dose of ethanol

A

produces gastric irritation,

causes back diffusion of acid from the gastric lumen into mucosa causing injury

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15
Q

who should avoid ethanol

A

peptic ulcer patient

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16
Q

ethanol caues vomiting

A

by central and local gastric effects,

commonly death occurs due to suffocation from inhaled vomitus

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17
Q

ethanol and sex

A

stimulates sexual desire and gives false confidence

but impairs the sexual performance

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18
Q

Ethanol chronic ingestion may lead to

A

impotence,
sterility,
testicular atrophy,
gynecomastia

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19
Q

feminization in alcoholic man has dual origin

A

alcohol induced hepatic injury leads to hyper estrogenization and decreased production of testosteron, increased metabolic inactivation of testosterone - genital shrinkage may occur in men

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20
Q

ethanol on glucose metabolism

A

inhibits gluconeogenesis and

hence produces fasting hypoglycemia

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21
Q

ethanol on uterus

A

relaxes uterus

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22
Q

ethalol and hyperuricemia

A

may lead to gout (lactate competes with urate for excretion)

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23
Q

ethanol effects on CVS - French Paradox

A

refers to the fact that people in France suffer relatively low incidence of coronary heart disease, despite having a diet relatively rich in saturated fats

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24
Q

ethanol on coronary diseases with low dose

A

small dose daily decreases coronary artery disease, alcohol increases level of HDL preventing atherosclrosis, low dose alcohol yields cardio protective effects (decreased risk of CHD compared to abstainer)

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25
Q

ethanol on coronary diseases with high dose

A

high dose of alcolol causes arrhythmia, cardiomyopathy, hemorrhagic stroke, alcohol has a J-shaped dose mortality curve

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26
Q

consumed at 1-20g/day to 21-40g/day results in

A

lower rates of angina pectoris, MI and peripheral artery disease

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27
Q

ethanol and hypertention

A

heavy alcohol use increases both diastolic and systolic BP

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28
Q

ethanol and arrhythmias

A

both atrial and vetricular arrhythmias

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29
Q

ethanol and cardiomyopathy

A

depresses cardiac contractility and leads to cardiomyopathy

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30
Q

ethanol effects on liver

A

fatty liver, alcoholic hepatitis, finally cirrhosis and liver failure

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31
Q

ethanol and cancer

A

increased risk of canser with chronic use of
mouth,
pharynx,
larynx,
esophagus, and
liver;
also small risk of breast cancer ——>due to the acetaldehyde metabolite!!

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32
Q

ethano absorption

A

very good and rapid oral absorption withing 5-10 min

– presence of food in gut delays absorption

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33
Q

peak concentration of ethanol reaches withing

A

30 to 90 minutes form the last drink

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34
Q

ethanol distribution in the body

A

fairly uniformly distributed throught all tissues and all fluids

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35
Q

ethanol is subject to gastric first pass metabolism by

A

alcohol dehydrogenase in the gastric wall

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36
Q

female and alcohol dehydrogenase

A

females have less alcohol dehydrogenase,

alcohol attains higher concentration in systemic blood for the same dose per Kg than in men.

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37
Q

liver and ethanol elimination

A

liver unusually plays a little role in presystemic elimination although it has a major role in its subsequent metabolism

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38
Q

placenta and alcohol

A

placenta is permeable to ethanol and henc reach fetus (fetal alcohol syndrome)

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39
Q

more than 90% of ethanol is oxidized in

A

the liver - micorsomal oxidation

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40
Q

elimination of alcohol follows

A

zero order kinetics –when the concentration in blood exceeds 10mg/100ml

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41
Q

alcohol leads to tolerance by

A

enzyme induction

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42
Q

ethanol degradation

A

ethyl alcohol

  • -> acetaldehyde (via alcohol dehydrogenase)
  • ->acetic acid (via acealdehyde dehydrogenase)
  • ->CO2 and H2O
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43
Q

pathways of ethanol metabolism through two ways

A

alcohol dehydrogenase path in cytosol,

microsomal ethanol oxidizing system (MEOS) located in the smooth endoplasmic reticulum

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44
Q

fomepizole

A

inhibits alchol dehydrogenase

–substrate can be ethanol or methanol

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45
Q

drug that inhibits alcohol dehydrogenase

A

fomepizole

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46
Q

drug that inhibits aldehyde dehydrogenase

A

disulfiram

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47
Q

disulfiram

A

inhibits aldehyde dehydrogenase

48
Q

principle path of alcohol metabolism

A

alcohol dehydrogenase path

49
Q

alcohol dehydrogenase path produces

A

acetaldehyde from alcohol,

NADH is also generated during the proces

50
Q

rate of ethanol oxidation is determined by

A

the capacity of the liver to re-oxidize NADH

51
Q

oxidation of ethanol in the liver

A

generates an excess of NADH

52
Q

if the ability of the hepatocytes to meaintain redox homeostasis is overwhlemed

A

then a number of metabolic distrubances arise including
lactic acidosis,
hyperuricemia, and
abnormalities of hepatic lipid metabolism

53
Q

MEOS (isoform of cytochrome P450) role in ethanol concentration below 100mg%

A

small

54
Q

MEOS induction

A

chronic alcohol use is associated with an increase in the metabolic rate for ethanol as a result of induction of MEOS system, can account for up to 10% of ethanol oxidation

55
Q

disulfiram inhibiting aldehyde dehydrogenase

A

increase acetaldehyde producing unpleasant symptoms so if taking disulfiram or drugs like it you don_t want to consume more

56
Q

treatment of methanol

A

ethanol cuts methanol bec alcohol dehydrogenase has higher affinity for ethanol so there is less production of fromaldehyde

57
Q

ethanol is mainly excreted through

A

urine, but also through
lungs and
sweat

58
Q

trigeminal neuralgia

A

ethanol is a last resort treatment for intractable trigeminal neuralgia

59
Q

repeated use of alcohol results in

A

tolerance –> physical dependence

(inc of dopamine release from the mesolimbic reward system)

60
Q

alcohol give more calories than carbs or protein

A

7g vs 4 g

61
Q

addictive cycle of alchohol

A

alcohol consumption

  • ->alcohol high - stimulation of opiod receptors
  • ->alcohol high diminishes, increasing desire for more stimualtion of opiod receptors
  • -> motivated to consume more alcohol–increased craving and loss of control
  • ->leads to more alcohol consumption
62
Q

cross tolerance with alcohol

A

benzodiazepines and
other CNS depressants

–>dangerous combination

63
Q

alcohol withdrawl syndrom

A

sudden stoppage in chronic consumer leads to alcohol withdrawal syndrome

64
Q

symptoms of alcohol withdrawl syndrom

A 
alcohol craving, 
tremors, 
irritability, 
nausea, 
sleep distrubances, 
tachycardia, 
inc in BP, 
sweating, 
perceptual distortion, 
hallucinations, 
seizures, 
Delirium Tremens, 
can be fatal
65
Q

fever and alcohol

A

vasodialation to dec temperature

66
Q

delirium tremens (severe)

A

refers to delirium (mental confusion, agitation, and fluctuation levels of consciousness)

associated with a tremor and autonomic overactivity (eg. Marked increases in pulse, bp, respirations)

–>severe agitation, confusion, visual hallucinations, fever, profuse sweating

67
Q

rubefacient

A

vasodialation so produced redness – rubbing it produces counter irritation

68
Q

Alcoholism

A

acute and chronic

69
Q

Acute alcoholism/intoxication

A

usually occurs in non-tolerant individuals who rapidly consume alcohol in large quantities;
normally the user passes out before a toxic dose of alcohol can be ingested;
the person vomits to rid the stomach of its toxic reservoir;
with rapid dringing the person may fall asleep or pass out without vomiting, allowing continued alcohol absroption form the GIT while the patient sleeps until fatal BAC are achieved

70
Q

S/S of acute alcoholism

A 
hypotension, 
tachycardia, 
hypoglycemia, 
respiratory depression, and 
coma
71
Q

when is alcohol fatal

A

more than 400mg/dl concentration

72
Q

treatment goal of acute alcoholism

A

to prevent severe respiratory depression and aspiration of vomitus

73
Q

Measures in acute alcoholism

A

maintenance of ABC,
gastric lavage,
treatment of hypoglycemia and ketsis by administration of IV glucose,
electrolyte balance,
treatment of violent behaviour –by sedatives and antipsychotics in low dose

74
Q

Chronic alcoholism may cause

A

malnutrition,

organ failure

75
Q

Malnutrition related to chronic alcoholism

A

partidulary def of B group vitamins (esp. thiamine, vit B1),
thiamine supplementation is standard therapy bc it can prevent the development of the Wernicke-Korsakoff Syndrom
(eg. Mental confusion, nystagmus, and ataxia)
which may not be reversible once developed

76
Q

organ damage related to chronic alcoholism

A

liver cirrhosis,
deteriorate bain fn (psychotic state, dementia, seizures, loss of memory etc),
peripheral neuropathy,
cardiomyopathy,
cancer of upper alimentary tract and resp tract,
hypertension

77
Q

abrupt withdrawl of alcohol leads to

A 
a characteristic syndrom of 
motor agitation, 
anxiety, 
insomnia and 
reduction of the seizure thrshold
78
Q

management of chronic alcoholism by detoxification

A

substituting a long-acting sedative hypnotic drugs for alcohol and then gradually reducing (tapering) the dose of the long-acting drug

79
Q

long acting BZDs include

A

chlordiazepoxide,

diazepam

80
Q

what is the advantage of the long acting bzs

A

less frequent dosing

81
Q

in pts with liver disease short acting bzds

A

oxazepam,

lorazepam

82
Q

fixed schedule therapy

A

psychological therapy,

aversion therapy

83
Q

drugs in aversion therapy

A

disulfiram (antabuse),

naltrexone

84
Q

disulfiram (antabuse)

A

aldehyde dehydrogenase inhibitor –renders alcohol unpleasant

85
Q

naltrexone (opiod antagonist) and Acamprosate (an analog of Gaba)

A

NMDA antagonist - helps in alcoholism by decreasing relapse and craving

86
Q

combination of disulfiram and naltrexone should have been avoided bc

A

both drugs are potential hepatotoxic

87
Q

disulfiram (antabuse) reactions

A 
facial flushing, 
throbbing headache, 
nausea, 
vomiting, 
sweating, 
hypotension, 
palpitation, 
tachycardia
88
Q

usual oral dose of Disulfiram

A

250mg daily

89
Q

other drugs producing disulfiram like reactions are

A 
metronidazole, 
chlorpropamide, 
griseofulvin, 
moxalactam, 
cefoperazone, 
cefotetan
90
Q

inhib of Alcohol dehydrogenase

A

cns depression,
metabolic acidosis,
acetaldehyde toxicity

91
Q

with increasing ethanol levels you get

A 
inc socialbility, 
gait disturbances, 
inc reaction time, 
ataxia, 
impaired motor and mental skills, 
impaired memory, 
coma, 
death
92
Q

inc acetaldehyde you get

A 
N &V, 
headache, 
hypotension, 
combines with folate to inactivate it, 
combines the thiamine to decrease availability
93
Q

disulfiram inhibits

A

acetaldehyde dehydrogenase in the mitochondria

94
Q

chronic alcoholism will show

A

hypoglycemia,
fatty liver and lipemia,
muscle wasting (long term alcoholic, poor food intake),
gout (lactate competes with urate for excretion)

95
Q

ethanol intoxication symptoms

A 
ataxia, 
nystagmus, 
sedation, 
flushed face, 
mood changes, 
impaired attention
96
Q

ethanol withdrawl symptoms

A 
tremors, 
hallucinations, 
insomnia, 
seizures, 
hyperthermia, 
nausea/vomitting
97
Q

Fetal alcohol syndrom

A 
chronic maternal alcohol abuse during pregnancy has teratogenic effects on the offspring like 
retarded body growth, 
microcephaly, 
poor co-ordination, 
hyperactive behavior
98
Q

what is a leading cause of mental retardation and congenital malformation in the US

A

fetal alcohol syndrome

99
Q

featurs of fetal alcohol syndrome

A 
flattened face, 
mid facial and mandibular growth deficiencies, 
mental retardation, 
minor joint anomalies, 
malfunction of organ systems like 
--skeltal, 
--CVS, 
--renogenital
100
Q

what is the vulnerable period for fetal alcohol syndrome

A

4 to 10 weeks

101
Q

pregnancy is unlikely to occur in

A

severly alcoholic women

102
Q

spontaneous miscarriage rate increases in

A

2nd trimester

103
Q

fetal liver alcohol dehydrogenase activity

A

no/little alcohol dehydrogenase activity

104
Q

guidelines for safe drinking

A

less than 2 drinks per day,
not more than 2 drinks on any occasion,
do not engage in hazardous activities after drinkin,
if contraindications do not drink,
do not drink if interacting drug is taken,
women to take less amt per kg

105
Q

other types of alcohol

A 
ethylene glycol (antifreeze agent, coolant), 
methanol (wood alcohol)
106
Q

methanol metabolism produces

A

formaldehyde and formic acid

107
Q

S/S accociated with methanol

A

respiratory failure,
severe anion gap metabolic acidosis,
ocular damage

108
Q

methanol toxic dose leading to blindness

A

5-10ml

109
Q

methanol toxic dose leading to death

A

30ml

110
Q

methanol is a major componet of

A

illicit liquor (moon-shining, boot-legging),
gasoline additive,
industrial solvent xerographic copier solutions

111
Q

methanol is absorbed from

A

the reps tract,
gi tract, and
skin

112
Q

formic acid can convert to

A

CO2 and water by folate-dependant pathway

113
Q

clinical features of methanol poisoning

A 
severe malaise, 
vomiting, 
abdominal pain, 
tachypnea, 
restlessness, 
headace, 
acidosis, 
blindness (like being in a snow storm), 
coma, 
circulatory collapse
114
Q

management of methanol poisoning

A 
put the patient in a dark room, 
support respiration, 
gastric lavage, 
nutrition and electrolytes, 
correct acidosis (IV NaHCO3), 
inhibit methanol metabolism, 
eliminate methanol and its metabolites by dialysis, 
admin of Ca - luecovorin
115
Q

what can you give to inhibit methanol metabolism

A

fomepizole (long acting inhibitor of alcohol dehydrogenase),
IV ethanol

Pharmacology 2 (12 decks)

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